- •Preface
- •Contributors
- •Dedication
- •INFECTIOUS DISEASES
- •ACINETOBACTER
- •BACILLUS SPECIES INFECTIONS
- •ESCHERICHIA COLI
- •GONOCOCCAL OCULAR DISEASE
- •INFECTIOUS MONONUCLEOSIS
- •MICROSPORIDIAL INFECTION
- •MOLLUSCUM CONTAGIOSUM
- •MORAXELLA
- •PROPIONIBACTERIUM ACNES
- •PROTEUS
- •PSEUDOMONAS AERUGINOSA
- •STREPTOCOCCUS
- •VARICELLA AND HERPES ZOSTER
- •PARASITIC DISEASES
- •PEDICULOSIS AND PHTHIRIASIS
- •NUTRITIONAL DISORDERS
- •INFLAMMATORY BOWEL DISEASE
- •DISORDERS OF CARBOHYDRATE METABOLISM
- •MUCOPOLYSACCHARIDOSIS IH
- •MUCOPOLYSACCHARIDOSIS IH/S
- •MUCOPOLYSACCHARIDOSIS II
- •MUCOPOLYSACCHARIDOSIS III
- •MUCOPOLYSACCHARIDOSIS IV
- •MUCOPOLYSACCHARIDOSIS VI
- •MUCOPOLYSACCHARIDOSIS VII
- •DISORDERS OF LIPID METABOLISM
- •HEMATOLOGIC AND CARDIOVASCULAR DISORDERS
- •CAROTID CAVERNOUS FISTULA
- •DERMATOLOGIC DISORDERS
- •ERYTHEMA MULTIFORME MAJOR
- •CONNECTIVE TISSUE DISORDERS
- •PSEUDOXANTHOMA ELASTICUM
- •RELAPSING POLYCHONDRITIS
- •UVEITIS ASSOCIATED WITH JUVENILE IDIOPATHIC ARTHRITIS
- •WEGENER GRANULOMATOSIS
- •WEILL–MARCHESANI SYNDROME
- •SKELETAL DISORDERS
- •PHAKOMATOSES
- •NEUROFIBROMATOSIS TYPE 1
- •STURGE–WEBER SYNDROME
- •NEUROLOGIC DISORDERS
- •ACQUIRED INFLAMMATORY DEMYELINATING NEUROPATHIES
- •CREUTZFELDT–JAKOB DISEASE
- •NEOPLASMS
- •JUVENILE XANTHOGRANULOMA
- •LEIOMYOMA
- •ORBITAL RHABDOMYOSARCOMA
- •SEBACEOUS GLAND CARCINOMA
- •SQUAMOUS CELL CARCINOMA
- •MANAGEMENT OF SCLERAL RUPTURES 871.4 AND LACERATIONS 871.2
- •IRIS LACERATIONS 364.74, IRIS HOLES 364.74, AND IRIDODIALYSIS 369.76
- •ORBITAL IMPLANT EXTRUSION
- •SHAKEN BABY SYNDROME
- •PAPILLORENAL SYNDROME
- •ANTERIOR CHAMBER
- •CHOROID
- •ANGIOID STREAKS
- •CHOROIDAL DETACHMENT
- •SYMPATHETIC OPHTHALMIA
- •CONJUNCTIVA
- •ALLERGIC CONJUNCTIVITIS
- •BACTERIAL CONJUNCTIVITIS
- •LIGNEOUS CONJUNCTIVITIS
- •OPHTHALMIA NEONATORUM
- •CORNEA
- •BACTERIAL CORNEAL ULCERS
- •CORNEAL MUCOUS PLAQUES
- •CORNEAL NEOVASCULARIZATION
- •FUCHS’ CORNEAL DYSTROPHY
- •KERATOCONJUNCTIVITIS SICCA AND SJÖGREN’S SYNDROME
- •LATTICE CORNEAL DYSTROPHY
- •NEUROPARALYTIC KERATITIS
- •PELLUCID MARGINAL DEGENERATION
- •EXTRAOCULAR MUSCLES
- •ACCOMMODATIVE ESOTROPIA
- •CONVERGENCE INSUFFICIENCY
- •MONOFIXATION SYNDROME
- •NYSTAGMUS
- •EYELIDS
- •BLEPHAROCHALASIS
- •BLEPHAROCONJUNCTIVITIS
- •EPICANTHUS
- •FACIAL MOVEMENT DISORDERS
- •FLOPPY EYELID SYNDROME
- •MARCUS GUNN SYNDROME
- •SEBORRHEIC BLEPHARITIS
- •XANTHELASMA
- •GLOBE
- •BACTERIAL ENDOPHTHALMITIS
- •FUNGAL ENDOPHTHALMITIS
- •INTRAOCULAR PRESSURE
- •ANGLE RECESSION GLAUCOMA
- •GLAUCOMA ASSOCIATED WITH ELEVATED VENOUS PRESSURE
- •GLAUCOMATOCYCLITIC CRISIS
- •NORMAL-TENSION GLAUCOMA (LOW-TENSION GLAUCOMA)
- •IRIS AND CILIARY BODY
- •ACCOMMODATIVE SPASM
- •LACRIMAL SYSTEM
- •LACRIMAL HYPOSECRETION
- •DISLOCATION OF THE LENS
- •LENTICONUS AND LENTIGLOBUS
- •MICROSPHEROPHAKIA
- •MACULA
- •CYSTOID MACULAR EDEMA
- •EPIMACULAR PROLIFERATION
- •OPTIC NERVE
- •ISCHEMIC OPTIC NEUROPATHIES
- •TRAUMATIC OPTIC NEUROPATHY
- •ORBIT
- •EXTERNAL ORBITAL FRACTURES
- •INTERNAL ORBITAL FRACTURES
- •OPTIC FORAMEN FRACTURES
- •RETINA
- •ACQUIRED RETINOSCHISIS
- •ACUTE RETINAL NECROSIS
- •DIFFUSE UNILATERAL SUBACUTE NEURORETINITIS
- •RETINOPATHY OF PREMATURITY
- •SCLERA
- •SCLEROMALACIA PERFORANS
- •VITREOUS
- •VITREOUS WICK SYNDROME
- •Index
●The lens changes may occur almost immediately or may take several years; the average time of onset is 2 to 6 months after injury.
●If only a few vacuoles are present in the anterior lens cortex within the first few weeks postinjury, there is a high probability that no significant cataract-one requiring surgerywill occur.
Part of the injury may be heat-related as much as it is true electrical damage secondary to contact between the iris and the lens. Retinal damage is more likely to be a thermal injury unless the exit point of the electrical injury indicated that the electrical current passed through the posterior segment of the eye.
DIAGNOSIS
Dilated-eye examination of both the lens and retina is necessary.
REFERENCES
Biro Z, Pamer Z: Electrical cataract and optic neuropathy. Int Ophthalmol 18:43–47, 1994.
Cooper MA: Treatment of lightning injury. In: Andrews CJ, Cooper MA, Darveniza M, Mackerras D, eds: Lightning injuries: electrical, medical, and legal aspects. Ann Arbor, MI, CRC, 1992:130–132, 1992.
Fraunfelder FT, Hanna C: Electric cataracts. I. Sequential changes, unusual and prognostic findings. Arch Ophthalmol 87:179, 1972.
Fraunfelder FT, Meyer SM: Treatment of lightning injury: special aspects of ocular management. In: Andrews CJ, et al: Lightning injuries: electrical, medical, and legal aspects. Boca Raton, CRC, 1992.
Grover S, Goodwin J: Lightning and electrical injuries: neuro-ophthalmo- logic aspects. Seminars in Neurology 15(4):335–341, 1995.
Hanna C, Fraunfelder FT, Johnston GC: Electrical-induced cataracts. Arch Ophthalmol 84:232, 1970.
Hanna C, Fraunfelder FT: Electric cataracts. II. Ultrastructural lens changes. Arch Ophthalmol 87:18, 1972.
Saffle JR, Crandall A, Warden GD: Cataracts: a long-term complication of electrical injury. J Trauma 25:17–21, 1985.
TREATMENT
Systemic
●Analgesics and tranquilizers are often required.
●Tetanus toxoid is administered if the patient has not had a booster within the past year.
●Antibiotics such as gentamicin 3 mg/kg or IM in three doses may be considered if necrotic tissue is present so as to decrease opportunistic bacteria.
154 MANAGEMENT OF SCLERAL RUPTURES 871.4 AND LACERATIONS 871.2
Ferenc Kuhn, MD, PhD
Birmingham, Alabama
Ocular |
ETIOLOGY |
●Try to maintain a cool, dry, clean wound environment.
●Clean periocular tissue regularly with diluted soap solution Ruptures are caused by large, blunt objects that exert pressure
or normal saline; this may have to be done b.i.d. to t.i.d.
●Apply periocular and ocular antibiotic ointments regularly.
●Try to keep burned areas open to the air if the lid can still cover the eye.
●Cycloplegics, such as 1% to 2% atropine qd to q.i.d. and dexamethasone 0.1% b.i.d. to q.i.d. may be necessary to control uveitis.
●As granulation tissue occurs, sterile dressings may be started.
Surgical
●If a cataract develops, lens extraction procedures are done as for nontraumatic cataracts.
●A split-thickness skin graft may be necessary for eyelid burns to protect the globe.
COMMENTS
Ocular injury secondary to electric shock or lightning may be thermal or electrical in its cause. Eyelid, conjunctiva, cornea, pupil, lens, retina, extraocular muscles, and central nervous system damage with secondary ocular effects may occur. Cataracts are the most common injury and usually appear within 3 to 6 months. Corneal and conjunctival injury are usually epithelial and subside after a few weeks. Usually, eyelid lesions are extensive only if the site of contact is close to the eye.
on the eye upon contact. As a result, the intraocular pressure (IOP) is raised, and eventually the eyewall’s resistance is overcome: the eye suffers an open globe injury. The eyewall opens where it’s the weakest, not necessarily at the point of contact. The most likely sites of rupture are at the limbus, at the insertion of the extraocular muscles and along previous (surgical or traumatic) wounds. Typically, there is no entry of the object into the eye. Consequently, the risk of endophthalmitis is very low while the risk of tissue prolapse is high.
Lacerations are, as opposed to ruptures, caused by a sharp object that enters the eye at the point of contact. If the object remains inside the eye, it is an intraocular foreign body (IOFB) injury; if it leaves the eye via the same route it entered, it is a penetrating injury; if it leaves the eye via a different (exit) wound, it is a perforating injury.
Tissue prolapse is also common with lacerations, although a little less so than with ruptures. Endophthalmitis, on the other hand, is much more of a danger. The roughly 5% risk with penetrating trauma approximately doubles if it is an IOFB injury.
COURSE/PROGNOSIS
An open globe injury is likely to have a better prognosis if:
●The initial visual acuity is good;
●The wound is located anteriorly;
●The wound is small;
●The injury is caused by a sharp, rather than blunt, object;
●The object is not a missile.
Lacerations and Ruptures154 ScleralCHAPTERof Management •
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Injuries Nonmechanical and Mechanical • 14 SECTION
DIAGNOSIS
Clinical signs and symptoms
The diagnosis of an open-globe injury should always be considered in the setting of ocular trauma. A detailed history is paramount as is a thorough ophthalmic examination. Some presentations may be obvious, with uvea prolapsed into the wound, but in other situations the diagnosis may not be as apparent. The following findings should raise suspicion of an occult scleral rupture:
Findings on clinical examination:
●A suspicious history;
●Decreased visual acuity/afferent pupillary defect;
●Hemorrhagic chemosis;
●Peaked pupil;
●Abnormally deep or shallow anterior chamber;
●Decreased intraocular pressure (although may also be elevated);
●Media opacity: hyphema, cataract and vitreous hemorrhage.
Laboratory findings
Based on the history and clinical findings, additional studies may be required:
●Axial and coronal computed tomography (for confirming/ excluding intraocular and orbital foreign bodies, orbital fractures, and occult scleral ruptures).
●Ultrasound (rarely needed for retinal detachment or intraocular foreign bodies; may carefully be applied in experienced hands preoperatively, although intraoperative or postoperative use is more common).
●Surgical exploration may be necessary if presence of an open-globe injury cannot otherwise be excluded.
Differential diagnosis
Most signs and symptoms can occur in other conditions; history should help determine the traumatic origin.
PROPHYLAXIS
Although great strides have been made in the surgical instrumentation and techniques for the management of open-globe injuries, prevention would be the ideal situation. Reduction of ocular morbidity may be accomplished by educating patients about protective polycarbonate eyewear. This is especially important for patients who are at high risk, including those who are involved in certain recreational and occupational activities, and those who are monocular such as those who have already lost vision in the fellow eye because of previous ocular trauma.
TREATMENT
If risk factors for infection (soil contamination, an object of organic matter, and the presence of lens injury in persons over 50 years of age) are present, prophylactic intravitreal antibiotic injection is warranted; clinical signs of endophthalmitis demands immediate surgical intervention (typically complete vitrectomy with intravitreal as well as systemic and local antibiotic therapy). Otherwise, the following describes the ‘typical’ surgical approach.
Surgical treatment for ruptures
Management is primarily determined by the location of the wound. If the wound is anterior (i.e. easily accessible to the surgeon), the prolapsed tissue must be dealt with first. If it is iris, it is usually cleaned – using forceps, microsponge (e.g. Weck Spears), or irrigation – and then reposited. Only iris that cannot be adequately cleaned of contamination or debris (e.g. epithelial cells), or that is necrotic should be excised. If the wound is at the limbus, iris reposition should be done via ‘pulling’ rather than ‘pushing’: through a paracentesis created at 90 degrees or more away for increased maneuverability, and using a blunt tool such as a spatula. Prolapse of the ciliary body or choroid is much rarer as these tissues are quite elastic; in general, they should be reposited, not excised, to decrease the risk of hemorrhage and inflammation. If vitreous has prolapsed, it must always be excised. Conversely, retina is never excised but should be gently reposited. Viscoelastics can be used both for reposition and as a prevention against reprolapse.
Once there is no tissue between the wound lips, suturing can start. The order of suture placement primarily depends on convenience. Ideally and if the entire wound can be visualized (requiring careful dissection of the conjunctiva to ensure that the scleral wound does not continue beyond what appears to be its termination), the ‘50% rule’ applies: the first suture is in the middle of the wound, the next two in the middle of each of the now two sections (at 25% and 75%), etc. An absorbable suture such as vicryl suffices: by the time of suture absortion in a few weeks, the wound is firmly closed by scar formation.
If the wound is posterior, the entire approach changes. It may be impossible, even dangerous, to inspect the wound in its entirety before suture placement, as this threatens with additional tissue prolapse and expulsive choroidal hemorrhage. The ‘close-as-you-go’ technique is recommended: the scleral wound is closed anteriorly, before another section of the conjunctiva is opened posteriorly; the sclera is closed again and the process can be repeated as needed. An assistant may be needed to ensure gentle but adequate exposure using traction sutures or retractor (e.g. Schepens). On rare occasions, an extraocular muscle may have to be temporarily taken off to increase access to the wound and ease of suturing.
The wound may be so posterior that accessing it is not only difficult but dangerous, threatening with (further) tissue prolapse/hemorrhage. The significance of this complication is greater than the benefit offered by suture-closure. In such cases, the wound is to be left open; by an outside-in process, proliferative cells will enter the site and close the wound within hours or days. Conversely, while this process ensures timely wound closure of acceptable firmness, it usually involves instant or eventual retinal incarceration that must be dealt with secondarily.
Surgical treatment of lacerations
If infection is not present or its risk is not elevated, management of the injured eye can be staged. The wound is dealt with in a similar fashion as described above: wound toilette, management of tissue prolapse, and suture-closure. If the wound is corneoscleral, the limbus is closed first, followed by the corneal part (typically using 10-0 nylon sutures), while the scleral aspect comes last.
If an IOFB is present, it is usually removed through a surgical, not the traumatic, wound: this provides for more control and less iatrogenic trauma. Again, whether IOFB removal and vitrectomy in eyes with posterior segment IOFB are performed in the same sitting is determined by the threat of infection
282
versus the risk of intraoperative hemorrhage. In eyes with increased endophthalmitis risk or in a hostile medicolegal environment, comprehensive initial intervention is preferred; otherwise, the experience of the surgeon and the availability of the proper infrastructure (equipment/expertise/staff) should be weighted. Haste in IOFB removal does not compensate for inadequate or inappropriate surgery. Moreover, extraction of a posterior segment IOFB alone does not reduce the risk of infection: a complete vitrectomy must also be performed with (removal of the infected medium).
If the injury is perforating, management of the exit wound requires considerations similar to those mentioned with a posterior rupture. Surgical closure is advised only if it can be done without exerting so much extra pressure on the globe that would threaten with expulsive hemorrhage or tissue prolapse. If this cannot be avoided, the surgeon is better off leaving the wound open and wait for spontaneous closure.
This chapter does not describe the secondary management (often vitrectomy) of eyes with open globe injury.
Medical treatment
Regardless of injury type, the inflammation and the intraocular pressure must be aggressively controlled postoperatively.
COMPLICATIONS
Virtually any complication that exists may occur either as the result of the injury or of the intervention itself; the list of the most severe complications includes, among others, sympathetic ophthalmia, endophthalmitis, retinal detachment, and proliferative vitreoretinopathy. The treatment of these complications is beyond the scope of this chapter.
REFERENCES
Dalma J: Extrabulbar tissue prolapse. In: Kuhn F, Pieramici D, eds: Ocular trauma: principles and practice. New York, Thieme, 2002.
Kuhn F, Mester V, Morris R: A proactive treatment approach for eyes with perforating injury. Klin Monatsbl Augenheilk 221:622–628, 2004.
Kuhn F, Morris R, Witherspoon CD, et al: A standardized classification of ocular trauma terminology. Ophthalmology 103:240–243, 1996.
Lindsey JL, Hamill B: Scleral and corneoscleral injuries. In: Kuhn F, Pieramici D, eds: Ocular trauma: principles and practice. New York, Thieme, 2002.
155 INTRAOCULAR FOREIGN BODY:
COPPER 871.6
Fleming D. Wertz, III, MD
Burlington, Massachusetts
understandably low. During the past 150 years, the advent of sophisticated machinery in the workplace, on the battlefield, and in the hobbyist’s workshop has produced an environment in which the number of penetrating injuries caused by coppercontaining compounds has risen. During the United States Civil War, 1861 to 1865, the incidence of penetrating ocular injuries was 0.5%. This incidence rose slightly during World War I to between 3% and 4%. Thirty years later, statistics from World War II and the Korean War indicate the rate of penetrating ocular injuries had risen to 5% to 6%. The Vietnam War and the Israeli conflict resulted in a rate approaching 9% to 10%. These statistics reflect the effects of modern weapons designed to inflict maximum injury to combatants’ anatomy above the level of the waist.
In plants and mills, copper and copper alloys are commonly used in the manufacture and repair of numerous devices. Copper wire and electromechanical devices containing copper alloys are routinely found in the workshops used for hobbies and home repairs. Therefore, the potential for penetrating injuries involving copper compounds is widespread. The true incidence of copper-containing retained foreign bodies is lower during times of peace than times of war, directly reflecting the nature of the military-industrial process.
The presence of intraocular copper-containing foreign bodies can result in one or more of the following:
●Suppurative endophthalmitis;
●Recurrent nongranulomatous inflammation;
●Fibrous encapsulation;
●Local or widespread dissemination of copper in the eye.
These ocular responses result from the chemistry of the copper ion within the eye. A copper ion participates in two processes. The first is oxidation-reduction reactions. Because of a moderately low redox potential, a copper ion is a reagent for and catalyst of electron transfer from organic donors. Ascorbic acid is oxidized by a cuprous ion to produce hydrogen peroxide. This has been associated with vitreous syneresis and collapse. A copper ion participates in the formation of free radicals. The resultant superoxide and hydroxyl radicals attack polyunsaturated fatty acids, which results in lipid peroxidation and the formation of alkoxy and peroxy radicals. This may lead to:
1.The initiation of arachidonic acid metabolism that produces prostaglandins and leukotrienes, creating inflammation; and
2.The incapacitation and death of cells, which results from the radicals’ attack on lipid-containing cell membranes.
The latter contributes to progressive ocular dysfunction.
The second process of the ion occurs when copper complexes with key enzymes. The copper ion either displaces metal ions or alters the stereo configuration of the molecule, which generates altered intracellular metabolism. For example, copper inactivates carbonic anhydrase, and this results in decreased intraocular pressure.
ETIOLOGY/INCIDENCE
The increased incidence of intraocular copper-containing foreign bodies reflects the vocations and avocations of modern societies. Prior to the Industrial Revolution, before the changes in the engineering of weapons of war and the changes in the hobbies practiced by those with increased leisure time, the incidence of intraocular copper-containing foreign bodies was
COURSE/PROGNOSIS
The clinical course can be highly variable. It is dependent on the size, location and copper content of the foreign body. Larger foreign bodies offer more surface area from which to liberate copper ion. In theory, the greater the surface area the greater the reaction should be. However, if the foreign body is
Copper155Body:CHAPTERForeign Intraocular •
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Injuries Nonmechanical and Mechanical • 14 SECTION
located in the mid vitreous, away from vascularized tissue with a high oxygen tension, it may sit intact without inciting inflammation, or it may be quietly encapsulated. Locations near the retina and ciliary body are more prone to be associated with inflammation or copper dissemination or both. If the foreign body is an alloy containing less than 85% copper, there may be no reaction. The most intense reactions are associated with a copper content greater than 85%. Apart from the damage caused by the penetrating injury, acute chalcosis will present rapidly with inflammation, hypotony and deteriorating visual function. Without intervention, this may progress to visual loss from the sequela of intraocular inflammation or intraocular fibrosis and result in inoperable retinal detachment. Chronic chalcosis may present with low-grade intraocular inflammation, variable degrees of intraocular copper dissemination, and highly variable changes or no changes in visual function. However, the tendency is toward gradual diminution of vision and for the clinical picture of chalcosis to appear over months or years. Surgical intervention is the most direct therapy, and recent advances in techniques and instrumentation ensure the best possible outcome, even in complex cases.
DIAGNOSIS
Clinical signs and symptoms
Ocular
●Anterior chamber: cells and flare, hypopyon, hyphema, copper-colored metallic particles.
●Cornea: deep stromal deposits, Kayser–Fleischer ring (usually superior and/or inferior, but may be circumferential).
●Globe: endophthalmitis, phthisis.
●Iris: greenish tinge, poor response to mydriatics.
●Lens: brownish-red, small, round deposits on zonules, subluxation, sunflower cataract, yellow or copper tinge.
●Optic nerve: papillitis.
●Retina: copper-colored macular sheen, detachment, edema, gliosis, ‘gold-leaf’ granular deposits in macula or adjacent vessels in the posterior pole, hemorrhages.
●Sclera: abscess, softening.
●Vitreous: abscess, fibrillar degeneration, greenish-brown or reddish-brown deposits, opacity, organization.
●Other: decreased visual acuity, nonspecific color vision defects, variable isopter constriction in visual field testing, variable disturbance in the rod and cone amplitudes in the electroretinogram, variable elevation in rod and cone thresholds in dark adaptometry, ocular hypotension, secondary glaucoma, subconjunctival foreign body resulting from intraocular extrusion (rare), sympathetic ophthalmia (rare), encapsulation of the foreign body with possible simulation of growing intraocular tumor without evidence of chalcosis.
Laboratory findings
●Computed tomography to define and localize the presence of an intraocular foreign body.
●B-scan ultrasonography to define the status of the vitreous and retina as dictated by the clinical situation.
●Visual field, color vision, electroretinogram, dark adaptometry, as required.
●Radiographic spectrometry to define the presence of intraocular copper ions.
PROPHYLAXIS
Use of protective eyewear designed to reduce ocular injuries would nearly eliminate penetrating ocular injuries in the workplace, on the field of battle, and in the home workshop.
TREATMENT
Systemic
Endophthalmitis prophylaxis should be employed on a routine basis in the presence of acute penetrating wounds and retained foreign bodies.
Oral prednisone suppresses the general inflammatory response and inhibits the migration of polymorphonuclear leukocytes as well as the release of inflammatory modulating factors. It can be used to stem the intraocular inflammation in preparation for a surgical procedure.
Local
After the appropriate diagnostic tests, in cases of recent trauma, the first maneuvers are directed to the closure of an open globe. The closure of anterior or posterior segment lacerations is accomplished with standard techniques and equipment.
Surgical
Vitrectomy, with or without lensectomy and scleral buckle, and immediate removal of the retained foreign body are the two initial options of a surgeon; the choice will be determined according to the associated ocular injuries and the type of surgical repair required. Copper alloys with a copper content of 85% or greater may incite an acute inflammatory response, including fibrosis and foreign body encapsulation, particularly when sited adjacent to the ciliary body and retina. Prompt surgical removal may be necessary.
Other
Local steroids may be effective in suppressing the eye’s response to copper. Peribulbar dexamethasone has been shown to suppress both inflammation and the encapsulation of intraocular copper.
COMPLICATIONS
●Small, shiny retained foreign bodies may be observed.
●Corrosion of the foreign body’s surface may herald the appearance of inflammation and/or the deposition of intraocular copper; this may necessitate removal of the foreign body.
●Serial visual acuities, color vision, visual fields, dark adaptometry, and electroretinography, if needed, may be used to follow small retained foreign bodies. Foreign body removal would be indicated in cases of progressive deterioration in the monitored visual parameters.
●The potential exists for the development of cataract, hypotony, uveitis, and altered visual function.
●Late surgical repair may be associated with cataract, aphakia, retinal breaks and/or detachment, intraocular hemorrhage and infection.
REFERENCES
Gorodetsky R, Weinreb A, Zeimer R, et al: Noninvasive copper measurement in chalcosis, comparison with electroretinography and ophthalmoscopy. Arch Ophthalmol 95:1059–1064, 1977.
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McGahan MC, Bito LZ, Myers BM: The pathophysiology of the ocular microenvironment. II. Copper-induced ocular inflammation and hypotony. Exp Eye Res 42:595–605, 1986.
Mittag T: Role of oxygen radicals in ocular inflammation and cellular damage. Exp Eye Res 39:759–769, 1984.
Neubauer H: Ocular metallosis. Trans Ophthalmol Soc UK 99:502–510, 1979. The Montgomery Lecture.
Rosenthal AR, Eckhert C: Copper and zinc in ophthalmology. In: Karcioglu ZA, Sarper RM, eds: Zinc and copper in medicine. Springfield, IL, Charles C Thomas, 1980:595–609.
Rosenthal AR, Marmor MF, Leuenberger P, et al: Chalcosis: a study of natural history. Ophthalmology 86:1956–1959, 1979.
Sternberg P: Trauma: principles and techniques of treatment. In: Ryan S, Glaser B, eds: Retina. 2nd edn. St Louis, CV Mosby, 1994:3: 2351–2378.
Zeimer R, Gorodetsky R, Lahav M, et al: Experimental chalcosis: a comparison between in vivo and in vitro findings. Arch Ophthalmol 96:115–119, 1978.
156 INTRAOCULAR FOREIGN BODY: NONMAGNETIC, CHEMICALLY INERT 871.6
Howard Shann-Cherng Ying, MD, PhD
Baltimore, Maryland
Peter L. Gehlbach, MD, PhD
Baltimore, Maryland
Intraocular foreign bodies are often associated with severely injured eyes. The subset of penetrating ocular trauma involving nonmagnetic, chemically inert foreign bodies may, in selected cases, present an opportunity to avoid the additional damage of foreign body removal. When an intraocular foreign body is suspected, basic surgical principles apply, and all open globes should be closed. If the foreign body is chemically inert, inorganic, does not interfere with the visual axis, and is not in a place to cause ongoing mechanical injury, then the most prudent course of management may be to leave it in the globe. A diagnosis of inert foreign body is always tentative, pending observation over several years. Careful attention during this interval is required for early detection of the significant sequelae associated with these injuries. If at the time of injury doubt exists as to the nature of the foreign body and removal seems to be straightforward, then surgical removal is appropriate.
ETIOLOGY/INCIDENCE
●The National Eye Trauma System Registry estimates that the annual number of reported ocular and orbital injuries in the United States is 2.4 million, 20,000 to 68,000 of which are vision-threatening injuries. In a report from this registry, of 492 eyes with intraocular foreign bodies, 92% were in male patients, 50% of injuries occurred in the occupational setting, 94% of persons wore no protective eyewear, and 44 (8.9%) had nonmetallic foreign bodies. In contrast, a review of hospital records from three centers in Tehran during the Iran-Iraq War (1980–1988) found 767 eyes with intraocular foreign bodies and 90% non-magnetic foreign bodies, suggesting that occupational and combat eye trauma may not be comparable.
●If intracorneal foreign bodies are excluded, roughly one fifth of intraocular foreign bodies are confined to the anterior segment, with a greater percentage of metallic foreign bodies having the energy to penetrate into the posterior segment.
●In the occupational setting, glass is the most common nonmetallic inert intraocular foreign body; however, in the combat setting, stone and sand are more common. Penetrating injuries secondary to glass differ from those caused by the more common foreign body, steel, in a number of ways. They tend to occur in a younger age group, are more commonly bilateral, and frequently involve multiple foreign bodies. These injuries present unique challenges with regard to direct visualization, detection, and surgical removal.
DIAGNOSIS
History
●Injuries associated with the shattering of glass, hammering, high-speed machinery, explosions and blasts, projectile weapons, release of materials under pressure, and so forth may lead one to suspect that an intraocular foreign body is present.
●Pediatric patients more often present with injuries from projectile weapons or explosions, leading to a higher proportion of multiple nonmetallic IOFBs, and greater incidence of retinal damage.
●Once a foreign body has been discovered and localized, preliminary assessment of its potential to cause toxic damage must be made.
●In most instances this determination can be made based on the historical account of the injury. If a fragment of an object has entered the eye, analysis of the remaining portion reveals its chemical composition.
●Materials such as gold, silver, aluminum, platinum, tantalum, glass, stone, porcelain, pottery fragments, gunpowder, silicone, rubber and plastics are generally considered nonreactive.
●Iron, copper, cobalt, lead, nickel and zinc are considered reactive and may require immediate removal in order to prevent additional toxic injury, e.g. acute chalcosis.
●Photochromic glass is not inert in the eye.
Physical examination
●In some instances a foreign body may be visualized directly, and no ancillary studies are necessary. If visualization of any portion of the globe is obscured and a foreign body is suspected, then imaging studies must be performed.
●Plain radiography of the globe and orbit is the traditional technique for screening purposes and will determine the presence of most metallic and many nonmetallic foreign bodies; however the sensitivity may be as low as 40%.
●Ultrasonography is sensitive in locating foreign bodies but requires a skilled examiner as well as caution if an open globe is suspected. Open globes do not necessarily preclude ultrasonography, as stand-off techniques that transmit minimal pressure to the eye may be employed.
●Magnet-assisted ultrasonography is performed when the examiner advances a strong magnet toward the globe during ultrasonography. Movement of the foreign body indicates that it is magnetic.
●Computed tomography (CT) is an important diagnostic modality for detection and localization of suspected IOFBs. It is atraumatic and provides valuable information about the
Inert Chemically Nonmagnetic,156Body:CHAPTERForeign Intraocular •
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Injuries Nonmechanical and Mechanical • 14 SECTION
integrity of intraocular structures. It is also useful in cases involving multiple foreign bodies. Modern spiral CT scanning using 3-mm image sections may detect 0.5mm glass or stone IOFBs with excellent sensitivity. Certain nonmetallic foreign bodies, such as wood, are nearly isodense to intravitreal blood and may be difficult to detect with CT. Sensitivity in detection as well as accuracy in localization are increased when ultrasonography and CT are used concurrently.
●Magnetic resonance imaging (MRI) is now widely available
and may detect and localize some nonmetallic, radiolucent (<600 Hounsfield units) IOFB not visualized by CT. If there is any possibility that the foreign body may be metallic, MRI should not be performed because of possible movement or heating of the object. MRI, in the setting of penetrating ocular trauma, has had limited application because of the potential for secondary injury.
COURSE/PROGNOSIS
●Visual outcomes correlate with the presenting visual acuity and mechanism of injury. Globe perforations secondary to lacerations or blunt trauma tend to do poorly compared to perforations caused by small, sharp-edged intraocular foreign bodies that may cause less direct mechanical damage when entering the eye. Foreign bodies that are larger, toxic, and of higher energy, e.g. gunshot or air rifle, at impact tend to do poorly. Recent series have verified these findings and add the presence of retinal lesions or vitreous hemorrhage as additional predictors of poor outcome.
●Endophthalmitis is reported to occur in 6.8% of eyes containing nonmetallic foreign bodies, in 7.2% of eyes containing metallic foreign bodies and, surprisingly, in only 5.9% of eyes containing vegetative material. A delay in primary closure of the globe beyond 24 hours results in a 4-fold increase in the incidence of the development of endophthalmitis overall and a 6-fold increase in patients older than 50 years. Mulivariate analysis has shown that delay in primary repair, ruptured lens capsule, and dirty wound are the major predictors of post-traumatic endophthalmitis.
PROPHYLAXIS
Prophylaxis remains the best approach to all penetrating ocular injury. It can be promoted through:
●Public education;
●Identification and avoidance of high-risk activities or situations;
●The wearing of protective goggles.
TREATMENT
Ocular
●Prophylactic topical antibiotics are indicated in all patients. Gram-positive and gram-negative coverage is appropriate.
●Most patients with IOFB have an accompanying traumatic uveitis that requires treatment with topical steroids and cycloplegics. Although steroids may increase the risk of infection, the potential sequelae of the inflammation that accompanies these injuries generally requires their use.
●Topical cycloplegics are also beneficial, as they reduce discomfort by placing the ciliary body at rest, and they may decrease vascular permeability.
Surgical
●Attempts at removal should be undertaken only under conditions that provide excellent visualization. Removal is normally easier during a secondary procedure when hemorrhage has cleared and hemostasis has improved.
●Anterior segment foreign bodies are generally managed through limbal incisions. Intralenticular foreign bodies associated with cataract formation are managed with lensectomy. Occasionally, small intralenticular inert foreign bodies do not cause cataract formation and can be observed.
●If a decision is made to remove a foreign body that is embedded in either the vitreous or retina or is lying on the retinal surface, then a pars plana vitrectomy is performed and the foreign body is grasped with an appropriate forceps. The object is then carefully removed through an incision in the pars plana or, for certain large foreign bodies, through the original entry site.
●Removal of nonmagnetic subretinal foreign bodies may require retinotomy or gentle expression through the entry site with a forceps. If the foreign body is thought to be inert and there is concern about causing further tissue damage during its removal, it should be left in place and the patient’s status monitored for toxic or mechanical damage.
●Inert foreign bodies may become encapsulated when left in the globe. If secondary removal is attempted, the foreign body is first carefully dissected free from its encasement. This releases tractional forces that could result in iatrogenic injury to adjacent structures.
COMPLICATIONS
●Although in 26% of eyes containing IOFB, the vitreous has been reported to be culture-positive for bacteria, clinically manifest endophthalmitis following penetrating ocular injury is relatively uncommon. In eight studies published
between 1984 and 1989, the incidence of endophthalmitis ranged from 2.9% to 13.3%. The largest of these (n = 492), from the National Eye Trauma System Registry, reported an
incidence of 6.9%, consistent with the average incidence in the combined studies (n = 1420) of 6.8%.
●Presumably, the failure of culture-positive eyes to manifest clinically significant endophthalmitis is in part a result of current management.
●Even with ideal management, endophthalmitis remains a constant threat in the initial period of treatment. Increasing inflammation may be an indicator of incipient endophthalmitis. Fibrin, vitreous organization, and hypopyon are suggestive. The first posterior signs include a slight whitening of the retina and a subtle vasculitis.
●Even though the incidence of endophthalmitis is low, when it is present, its effects are often devastating. Therefore, a high index of suspicion must be maintained in all cases. When signs of endophthalmitis are present at the time of primary closure, cultures should be taken.
●Taking routine intraoperative bacterial cultures in patients without clinical indicators of endophthalmitis has not been shown to identify patients who will go on to develop
286
clinically significant endophthalmitis. The results of these cultures do not ordinarily serve to direct management decisions.
●All foreign bodies that are removed from the globe should be sent for culture and identification.
●Prophylactic intravitreal antibiotics in a prospective, doublemasked randomized study failed to show a statistical benefit for intraocular antibiotics although all 4 eyes (6.6%) with endophthalmitis were in the control group; however, some authors feel that they are indicated if the wound is particularly dirty or the foreign body originated in the soil or in a farm environment.
●In this setting, antibiotic coverage must include organisms of the Bacillus genus, which are commonly β-lactamase- positive. This virulent pathogen is usually sensitive to vancomycin and is often sensitive to aminoglycosides and clindamycin.
●It should be noted that intravitreal agents are them-
selves potentially toxic and the procedure is not without complications. Intravitreal injection should not be administered unless there is excellent visualization of the needle tip during the procedure. A slow injection, with the stream directed away from the macula, is recommended.
●Vigilant observation for the possible development of endophthalmitis is mandatory. Ongoing evaluation for possible late sequelae of IOFB injuries, including but not limited to cataract, retinal detachment, and unexpected toxicity from a foreign body, is essential. Secondary retinal detachment
with proliferative vitreoretinopathy was associated with poor initial visual acuity (<20/200) or vitreous hemorrhage and occurred in 11–13% of IOFB patients at 3.1–4.6 months after primary repair in two large cohorts. Prophylactic scleral buckling in a prospective, randomized study failed to show a statistical reduction in risk of secondary retinal detachment.
SUMMARY
Successful management of nonmagnetic, chemically inert intraocular foreign bodies requires a complete and comprehensive evaluation directed at:
●Assessing the extent of mechanical injury to the globe;
●Identifying and localizing all intraocular foreign bodies;
●Accurately assessing the foreign body’s potential for toxicity.
These cases demand a combination of conservatism and vigilance. Because removal may entail high-risk surgery without the advantage of magnetic extraction techniques, early management should be biased toward leaving small inert (both chemically nonreactive and mechanically bengin) foreign bodies undisturbed-with the following cautions:
●All open globes require closure;
●Long-term follow-up to monitor for late sequelae is required;
●Inert objects may still cause fibrous tissue proliferation with late contraction, resulting in epimacular proliferation or retinal detachment;
●Endophthalmitis can cause devastating destruction as a result of a seemingly minor wound;
●A diagnosis of inert foreign body is always tentative until it has been observed for several years.
REFERENCES
Azad RV, Kumar N, Sharma YR, Vohra R: Role of prophylactic scleral buckling in the management of retained intraocular foreign bodies. Clin Experiment Ophthalmol 32:58–61, 2004.
Brinton GS, Aaberg TM, Reeser FH, et al: Surgical results in ocular trauma involving the posterior segment. Am J Ophthalmol 93:271–278, 1982.
Bryden FM, Pyott AA, Bailey M, McGhee CN: Real time ultrasound in the assessment of intraocular foreign bodies. Eye 4(Pt 5):727–731, 1990.
Cardillo JA, Farah ME, Mitre J, et al: An intravitreal biodegradable sustained release naproxen and 5-fluorouracil system for the treatment of experimental post-traumatic proliferative vitreoretinopathy. Br J Ophthalmol 88:1201–1205, 2004.
Chiquet C, Gain P, Zech JC, et al: Risk factors for secondary retinal detachment after extraction of intraocular foreign bodies. Can J Ophthalmol 37:168–176, 2002.
Dass AB, Ferrone PJ, Chu YR, et al: Sensitivity of spiral computed tomography scanning for detecting intraocular foreign bodies. Ophthalmology 108:2326–2328, 2001.
de Juan E, Jr, Sternberg P, Jr, Michels RG: Penetrating ocular injuries. Types of injuries and visual results. Ophthalmology 90:1318–1322, 1983.
Essex RW, Yi Q, Charles PG, Allen PJ. Post-traumatic endophthalmitis. Ophthalmology 111:2015–2022, 2004.
Foster RE, Martinez JA, Murray TG, et al: Useful visual outcomes after treatment of Bacillus cereus endophthalmitis. Ophthalmology 103:390– 397, 1996.
Gopal L, Banker AS, Deb N, et al: Management of glass intraocular foreign bodies. Retina 18:213–220, 1998.
Greven CM, Engelbrecht NE, Slusher MM, Nagy SS: Intraocular foreign bodies: management, prognostic factors, and visual outcomes. Ophthalmology 107:608–612, 2000.
Gunenc U, Maden A, Kaynak S, Pirnar T: Magnetic resonance imaging and computed tomography in the detection and localization of intraocular foreign bodies. Doc Ophthalmol 81:369–378, 1992.
Heimann K, Paulmann H, Tavakolian U: The intraocular foreign body. Principles and problems in the management of complicated cases by pars plana vitrectomy. Int Ophthalmol 6:235–242, 1983.
Jonas JB, Knorr HL, Budde WM: Prognostic factors in ocular injuries caused by intraocular or retrobulbar foreign bodies. Ophthalmology 107:823– 828, 2000.
Khosla PK, Murthy KS, Tewari HK: Retinal toxicity of trace elements. Indian J Ophthalmol 35:311–314, 1987.
Mieler WF, Ellis MK, Williams DF, Han DP: Retained intraocular foreign bodies and endophthalmitis. Ophthalmology 97:1532–1538, 1990.
Neubauer H: The Montgomery Lecture, 1979. Ocular metallosis. Trans Ophthalmol Soc U K 99:502–510, 1979.
New PF, Rosen BR, Brady TJ, et al: Potential hazards and artifacts of ferromagnetic and nonferromagnetic surgical and dental materials and devices in nuclear magnetic resonance imaging. Radiology 147:139– 148, 1983.
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Parver LM, Dannenberg AL, Blacklow B, et al: Characteristics and causes of penetrating eye injuries reported to the National Eye Trauma System Registry, 1985–91. Public Health Rep 108:625–632, 1993.
Penner R, Passmore JW: Magnetic vs nonmagnetic intraocular foreign bodies. An ultrasonic determination. Arch Ophthalmol 76:676–677, 1966.
Pieramici DJ, MacCumber MW, Humayun MU, et al: Open-globe injury. Update on types of injuries and visual results. Ophthalmology 103:1798–1803, 1996.
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Rubsamen PE, Cousins SW, Martinez JA: Impact of cultures on management decisions following surgical repair of penetrating ocular trauma. Ophthalmic Surg Lasers 28:43–49, 1997.
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Rubsamen PE, Cousins SW, Winward KE, Byrne SF: Diagnostic ultrasound and pars plana vitrectomy in penetrating ocular trauma. Ophthalmology 101:809–814, 1994.
Soheilian M, Rafati N, Peyman GA: Prophylaxis of acute posttraumatic bacterial endophthalmitis with or without combined intraocular antibiotics: a prospective, double-masked randomized pilot study. Int Ophthalmol 24:323–330, 2001.
Thompson JT, Parver LM, Enger CL, et al: Infectious endophthalmitis after penetrating injuries with retained intraocular foreign bodies. National Eye Trauma System. Ophthalmology 100:1468–1474, 1993.
Williams DF, Mieler WF, Abrams GW: Intraocular foreign bodies in young people. Retina 10(Suppl 1):S45–S49, 1990.
157 INTRAOCULAR FOREIGN BODY:
STEEL OR IRON 871.5
Christophe Chiquet, MD, PhD
Grenoble, France
Gilles Thuret, MD, PhD
Saint-Etienne, France
Philippe Gain, MD, PhD
Saint-Etienne, France
Jean-Paul Romanet, MD
Grenoble, France
ETIOLOGY/INCIDENCE
Intraocular foreign bodies (IOFBs) are a major cause of ocular trauma (up to 40%) and of legal blindness. Young adults, especially men, are the most likely victims, as a result of industrial, agricultural or firearm injuries. IOFBs are most commonly steel or iron, and generally result from hammering metal-on-metal (up to 72%) or from injuries caused by machines. Between 55% and 80% of metallic IOFBs are magnetic.
DIAGNOSIS
●A history of a metal-on-metal or machine-related accident is suggestive of the presence of a foreign body.
●The most common perforation sites are the cornea (52%), the sclera (34%) and an association of cornea and sclera (15%). A scleral wound may be masked by a subconjunctival hemorrhage and thus unnoticed by the patient.
●The presence of an IOFB in the anterior segment is frequently associated with a corneal perforation, positive Seidel’s test, conjunctival laceration, hemorrhage or edema, hyphema, iris defect, or lens disruption with or without cataract formation. Gonioscopy may reveal a foreign body lodged in the anterior chamber angle.
●A posterior segment IOFB must be suspected if there are vitreous strands or hemorrhage, air bubbles, retinal hemorrhage, inflammation, or edema related to a retinal impact site. A posterior IOFB is sometimes encapsulated.
●Computerized tomography (CT) scanning has become the standard method for imaging ruptured globes and remains the most sensitive method for detecting metallic foreign bodies. CT scanning allows detection of IOFBs with diameters of 0.5 mm or more, can distinguish metallic from nonmetallic foreign bodies, and can identify the composition of many nonmetallic IOFBs. Moreover, CT evaluation of pen-
etrating ocular trauma can be used to predict functional and anatomic outcome in eyes with penetrating injuries.
●Ultrasonography is both sensitive and specific in evaluating traumatized eyes, in localizing the IOFB, and in identifying associated lesions (choroidal hemorrhage, posterior exit sites, retinal and posterior vitreous detachment).
●Magnetic resonance imaging is contraindicated, as it may cause a shift in the position of a magnetic IOFB.
TREATMENT
Infection prophylaxis
●Intravenous antibiotics are routinely recommended as prophylaxis against endophthalmitis. Broad-spectrum coverage with antibiotics (association of fluoroquinolones and fosfocine or piperilline) is commonly used.
●Intravitreal antibiotics may be used prophylactically, at the time of initial surgical repair or at admission if no surgery
is required prior to vitrectomy (vancomycin 1 mg with either ceftazidime 2.25 mg or amikacin 200–400 μg). They are particularly indicated if signs of endophthalmitis are present at the time of surgical repair or if the nature of the injury suggests a high risk of endophthalmitis developing.
Surgical
Closure of the entrance wound to restore integrity of the globe, and repositioning or removal of prolapsed uvea, are the first concern during primary surgery. The method of removal involving the least surgical trauma and greatest control is determined.
ANTERIOR SEGMENT INTRAOCULAR FOREIGN BODY
●An IOFB anterior to the lens may be approached through a limbal incision over the area of the foreign body or 180 degrees away.
●An anterior segment IOFB may be dislodged with a bent needle, pick, or intraocular forceps or by using magnet extraction.
INTRALENTICULAR FOREIGN BODY
●Depending on location and composition of the IOFB, it may be well tolerated indefinitely with little secondary lens change or may be associated with toxicity or cataractous lens changes necessitating IOFB removal (Figure 157.1).
●If cataract formation and/or IOFB toxicity is present, extracapsular cataract extraction or phacoemulsification may be accomplished. Anterior vitrectomy may be performed as needed for posterior capsule rupture.
●Aphakia may be corrected using posterior chamber intraocular lens (IOL) implantation, scleral or iris suture fixation of IOL, anterior chamber IOL implantation or contact lens correction.
POSTERIOR SEGMENT INTRAOCULAR FOREIGN BODY
After a 360° conjunctival peritomy, the sclera is explored and any corneoscleral wounds are closed with multiple interrupted sutures.
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FIGURE 157.1. Intralenticular IOFB: this metal foreign body is located in the lens and was complicated by cataractous changes. There is no intraocular inflammation at this time.
●Extraction using an external magnet:
●Careful localization of the IOFB before extraction is critical;
●A direct approach is possible for anteriorly located intraor subretinal magnetic IOFBs via scleral cutdown (generally a T-shaped configuration) adjacent to the IOFB;
●The indirect transvitreal approach may be attempted if the IOFB is magnetic, pre-retinal (without encapsulating
fibrous material) or within the vitreous and small in size (<3 mm diameter). This technique consists of placing the electromagnet at an extraction site on the pars plana; the magnet should be directed so that, as the IOFB is removed, it does not inadvertently damage the lens or retina.
●Extraction using pars plana vitrectomy (PPV):
●Vitreous surgery allows excellent visualization and removal of blood, lens materials, and organisms if present. It is the technique of choice for IOFB removal from the posterior segment, especially if the body is located in the retina, encapsulated, and/or associated with media opacities. Vitrectomy needs to be relatively complete. Attention to the removal of the posterior hyaloid to prevent later epiretinal membrane formation has been emphasized. However, in many young people, it may not be possible to remove a portion of the posterior vitreous cortex on the macula or the optic nerve;
●Delaying vitrectomy (by 5–10 days) in eyes without evidence of infection decreases the chance of intraoperative bleeding and allows spontaneous separation of the posterior hyaloid;
●Intraocular magnets can be used to pick up IOFBs for transfer to diamond-coated forceps and removal;
●An intraretinal IOFB may be extracted using forceps or a 20-gauge rare-earth magnet. Subretinal IOFBs are removed with the foreign body forceps via a retinotomy;
●For encapsulated IOFBs, after vitreous removal the fibrous capsule is incised with the MVR blade and removal of the top of the capsule with 20-gauge scissors allows the foreign body to be freed before removal;
●Retinopexy around a retinal impact site is rarely necessary, and its benefit is debatable. Excessive and unnecessary retinopexy leads to greater wound-related cellular proliferation and inflammation;
FIGURE 157.2. Siderosis: complicates ferric IOFB, located on the iris in this case. This complication must be suspected when IOFB is associated with discoloration of the cornea, iris, lens (note subanterior capsular deposits in this example). A prompt extraction of the IOFB is needed.
●Extraction may be accomplished via a limbal incision if lensectomy or phacoemulsification has been performed. Lens extraction may be necessary for the translimbal removal of a very large foreign body;
●Secondary PPV is performed for postoperative complications, such as persistent vitreous hemorrhage, epiretinal membranes and RD.
●Other routes of extraction:
●If the foreign body is in the choroid or sclera, extraction can be performed through a scleral trap door or a direct cutdown, using a forceps or magnet;
●If corneal damage necessitates a penetrating keratoplasty, an open-sky vitrectomy with foreign body removal can also be effective.
●No surgery and frequent follow-up:
●May be discussed for intralenticular IOFB;
●Submacular and intraoptic nerve foreign bodies should be managed on an individual basis because of the hazards of removal.
COMPLICATIONS
Siderosis
●Is the process of chronic intracellular damage resulting from
electrolytic dissociation or oxidation of elemental iron (Fe) to ferric (Fe3+) and ferrous (Fe2+) ions.
●Onset rapidity is determined by the location and iron content of the foreign body. Location has high prognostic significance, with a poorer visual outcome for posterior segment IOFBs (as compared to intralenticular or anterior segment IOFBs).
●May cause inflammation or hypopyon, rusty discoloration of the conjunctiva, the cornea (with corneal edema, Fleischer’s ring, a Hudson–Stähli line, interstitial keratitis, or corneal neovascularization), the iris (with iridoplegia, or synechiae), the lens (with subanterior capsular deposits : see Figure 157.2, luxation, or subluxation), and/or the retina (with arteriolar narrowing).
●May be complicated by retinal detachment (RD), macular edema, pigmentary degeneration, secondary glaucoma,
Iron or Steel157Body:CHAPTERForeign Intraocular •
289
Injuries Nonmechanical and Mechanical • 14 SECTION
dyschromatopsia, night blindness, visual loss, and phthisis bulbi.
●Electroretinography is a sensitive clinical measure of siderotic change and typically shows an initial supernormality with later slow decrease in b-wave amplitude. Abnormalities may be present before visual acuity is affected.
●Abnormalities in dark adaptation and electro-oculography have also been noted.
Endophthalmitis
Endophthalmitis remains a serious complication of IOFB injuries (2%–13%), and clinical signs (hypopyon, vitritis, retinal periphlebitis) may be masked in the acute phase after severe ocular injury, thereby making diagnosis difficult in some cases.
●The most organisms most commonly isolated are Staphylococcus, Streptococcus and Bacillus species.
●Risk factors include: a delay in primary repair, disruption of the crystalline lens, home or occupational injuries, contamination with organic matter.
●If diagnosis of endophthalmitis is probable, an injection of antibiotics in the vitreous must be performed at initial presentation, before early IOFB removal is then scheduled. This is combined with subconjunctival and fortified topical antibiotic administration and, in most cases, with at least a short course of systemic antibiotics as well.
Retinal detachment
●Preoperative RD is present in 5%–21% of patients.
●Postoperative RD occurs in 14%–37% of cases, mainly during the first four months after injury, and is a crucial factor in poor visual outcome after IOFB injury (final VA equal to or worse than 20/100 in 68%). Risk factors are firearm injury, size of IOFB, low initial visual acuity, vitreous prolapse and/or hemorrhage. Incidence of RD in patients with retinal IOFB is around 25%.
●Incidence of RD with proliferative vitreoretinopathy (PVR) is 20%. In patients with ocular trauma or IOFB, vitreous hemorrhage, persistent intraocular inflammation or a posteriorly located wound are independent predictive factors for the development of post-traumatic PVR. Severe vitreous hemorrhage is associated with intraocular fibroblastic proliferation and traction RD in experimental and clinical studies.
●To offset late vitreous base contraction, prophylactic scleral buckling has been suggested.
Others
Corneal decompensation (due to direct laceration or endothelial cell loss), glaucoma, pupillary membranes, ciliary body detachment (with subsequent hypotony), traumatic cataract, epiretinal membranes, choroidal hemorrhages (especially in eyes with IOFB lying deep within the choroid), focal granuloma formation in the choroid.
PROGNOSIS
Prognosis after IOFB removal is associated with:
●The nature of the injury: for example, prognosis is poor in the event of blunt injury, particularly when due to firearm accidents;
●IOFB characteristics, particularly size (the relative risk of poor visual outcome is multiplied by a factor of 1.21 with each IOFB size increase of 1 mm);
●Clinical data at initial presentation: poor visual acuity (VA), deficit of the pupil afferent reflex, presence of an hyphema, prolapse of intraocular tissue, lens injury, corneoscleral entry wound are indicators of poor final visual outcome;
●Post-operative RD.
Visual outcome is strongly influenced by the nature of the penetrating trauma and the extent of the initial wound(s). The percentage of patients with final VA better than or equal to 20/63 ranged from 39% to 66% in several studies.
COMMENTS
Steel or iron intraocular foreign bodies should be removed, particularly to prevent the possibility of siderotic damage. In recent decades microsurgical techniques have improved and IOFB management is better codified. Due to the magnetic nature of the foreign body, surgical removal may be performed using an external or a 20-gauge rare-earth magnet. Prognosis most often depends on the severity of the initial injury and on the development of secondary RD. Increased public awareness of the incidence of open-globe injuries in high-risk activities, and the promotion of safety glasses, should markedly decrease incidence of these injuries.
REFERENCES
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Ahmadieh H, Sajjadi H, Azarmina M, et al: Surgical management of intraretinal foreign bodies. Retina 14:397–403, 1994.
Ambler JS, Meyers SM: Management of intraretinal metallic foreign bodies without retinopexy in the absence of retinal detachment. Ophthalmology 98:391–394, 1991.
Behrens-Baumann W, Praetorius G: Intraocular foreign bodies. 297 consecutive cases. Ophthalmologica 198:84–88, 1989.
Chiquet C, Gain P, Zech JC, et al: Risk factors for secondary retinal detachment after extraction of intraocular foreign bodies. Can J Ophthalmol 37:168–176, 2002.
Chiquet C, Zech JC, Denis P, et al: Intraocular foreign bodies. Factors influencing final visual outcome. Acta Ophthalmol Scand 77:321–325, 1999.
Chiquet C, Zech JC, Gain P, et al: Visual outcome and prognostic factors after magnetic extraction of posterior segment foreign bodies in 40 cases. Br J Ophthalmol 82:801–806, 1998.
Coleman DJ, Lucas BC, Rondeau MJ, et al: Management of intraocular foreign bodies. Ophthalmology 94:1647–1653, 1987.
De Juan E, Jr, Sternberg P, Jr, Michels RG: Penetrating ocular injuries. Types of injuries and visual results. Ophthalmology 90:1318–1322, 1983.
Essex RW, Yi Q, Charles PG, et al: Post-traumatic endophthalmitis. Ophthalmology 111:2015–2022, 2004.
Greven CM, Engelbrecht NE, Slusher MM, et al: Intraocular foreign bodies: management, prognostic factors, and visual outcomes. Ophthalmology 107:608–612, 2000.
Jonas JB, Knorr HL, Budde WM: Prognostic factors in ocular injuries caused by intraocular or retrobulbar foreign bodies. Ophthalmology 107:823– 828, 2000.
Maguire AM, Enger C, Eliott D, et al: Computerized tomography in the evaluation of penetrating ocular injuries. Retina 11:405–411, 1991.
Mieler WF, Ellis MK, Williams DF, et al: Retained intraocular foreign bodies and endophthalmitis. Ophthalmology 97:1532–1538, 1990.
Mieler WF, Mittra RA: The role and timing of pars plana vitrectomy in penetrating ocular trauma. Arch Ophthalmol 115:1191–1192, 1997.
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