AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Phacoanaphylaxis/lens-induced uveitis occurs in the setting of a ruptured or degenerative lens capsule and is characterized by a granulomatous antigenic reaction to lens protein. Before the modern era of microsurgery, this disease was more common, and the diagnosis was often made histologically, as eyes with phacoanaphylaxis were often enucleated for intractable inflammation and secondary glaucoma.

With improved microsurgical techniques, especially with the introduction of extracapsular cataract extraction and phacoemulsification, the incidence of phacoanaphylaxis has decreased dramatically and rarely occurs in its originally described form. However, chronic postoperative uveitis following phacoemulsification with retained lens material is still a well-known complication of cataract surgery and is the result of the same pathophysiology as the classically described entity of phacoanaphylaxis.

While lens fragments may be retained in the anterior or posterior chamber during seemingly uncomplicated cataract surgery, they also may be dislocated posteriorly into the vitreous cavity during phacoemulsification of the nucleus, usually after zonular dehiscence or posterior capsule rupture. Lens-induced uveitis may develop, and the degree of intraocular inflammation in these patients often is governed by the size of the retained lens fragment, the time since cataract surgery, the patient's individual inflammatory response, and the extent of other intraocular manipulations.

Pathophysiology

Lens proteins are most likely immunologically privileged, and they may initiate an immunologic sensitization only after entering the aqueous humor. This privilege is probably because of numerous factors, as follows: lens proteins are isolated from the fetal circulation early in embryonic life, the lens is devoid of innervation, and the adult lens is completely avascular. However, the immunopathogenesis of lens-induced uveitis is not precisely understood.

Antigenicity of lens proteins

The lens is an epithelial structure as it is derived from primitive ectoderm. By virtue of its capacity to synthesize alpha crystallins, the lens epithelium may become strongly antigenic. The protein concentration within the lens is higher than that of any other tissue in the body.

Early experiments inferred that lens antigens are shared among a number of animal species, and they can provoke the formation of homologous antibodies. Halbert et al found that lens proteins might be autoantigenic when they escape from their position of immunological isolation in the lens capsule. Each of the crystallin protein groups of lens cortical fibers contains a number of subtypes with distinct antigenic characteristics. Autologous lens proteins are only weakly antigenic, but fractionated crystallins are much more effective in stimulating an antibody response. The conversion process from soluble crystallins to insoluble proteins during aging of the lens also may result in an increased antigenic effect of proteins from mature or hypermature cataracts.

Histopathology

The classic histologic picture is one of zonal granulomatous inflammation. Polymorphonuclear leukocyte infiltration around degenerate lens remnants is surrounded by a palisade of macrophages, including epithelioid cells and multinucleated giant cells (see Images 1-3). Eosinophils may be prominent, and, eventually, fibroblastic granulation tissue develops together with prominent lymphocyte and plasma cell infiltration. The uveitis principally affects the iris, with the choroid being only secondarily involved. Retinal perivasculitis and papillitis may develop because of the presence of cross-reacting antigens in these tissues. Although a zonal granulomatous inflammation is the classic histopathologic description, a nongranulomatous uveitis also has been observed (see Image 4).

Pathogenesis

The term phacoanaphylaxis is probably inappropriate because no evidence exists of a classic type I immunoglobulin E (IgE) mediated anaphylactic reaction. The immunopathogenesis of lens-induced uveitis is believed to be the result of autosensitization to lens proteins. After a break in the lens capsule and sensitization to lens proteins, an immune complex–mediated phenomenon develops, which can be transferred by hyperimmune serum. Type II, III, and IV hypersensitivity reactions may be involved in the pathogenesis.

The disease most likely is induced by altered tolerance to lens protein and not as a result of a rejection phenomenon of sequestered foreign materials. The specific type of immunological reaction in lens-induced uveitis may vary from patient to patient, and it may depend on the type of surgery or injury, the amount of retained lens in the vitreous cavity, and the previous immunological status of both the patient and the eye.

Frequency

United States

Same as internationally.

International

The incidence of both phacoanaphylaxis and lens-induced uveitis is unknown. The best estimate of the incidence of posteriorly displaced lens fragments during phacoemulsification is 0.3-18% (the latter figure reported by a surgeon learning to use phacoemulsification). The incidence of retained lens fragments has increased as phacoemulsification has become more popular for cataract surgery. Although data are lacking, the authors' clinical impression is that about 50% of patients with retained lens material after cataract surgery have lens-induced uveitis. The incidence of lens-induced uveitis following penetrating injury is unknown.

Mortality/Morbidity

Lens-induced uveitis may cause or may be associated with cystoid macular edema, hypotony, phthisis, and secondary glaucoma. Complications also may be the result of medical or surgical treatment of lens-induced uveitis.

Race

No racial predilection exists.

Sex

No sexual predilection exists.

Age

Phacoanaphylactic endophthalmitis and lens-induced uveitis are more common in the elderly population, with a peak incidence in the sixth to seventh decades. The main exception is traumatic cataract and related complications, which are more common in younger age groups.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Phacoanaphylactic uveitis/lens-induced uveitis typically develops 1-14 days after traumatic or surgical perforation of the lens capsule. In rare instances, the inflammation may develop several months after the disruption of the lens capsule. In the large pathologic study by Thatch and Marak, there was no history of trauma or histopathologic evidence of a penetrating wound in about 20% of cases where phacoanaphylaxis was verified histopathologically.

• Clinical symptoms may include severe light sensitivity, epiphora, pain, floaters, decreased vision, and redness of the eye.
• Decreased vision may be due to refractive error (myopic or hyperopic shift) associated with such factors as macular edema, hypotony, or change in lens position.
• Visual acuity in patients with phacoanaphylactic uveitis is quite variable, ranging from 20/20 to no light perception.

Physical

Typically, the onset of lens-induced uveitis occurs 1-14 days after traumatic or surgical capsular disruption. However, unusual cases have been reported where the reaction occurred as early as several hours or as late as several months following capsular rupture.

• The inflammation can vary from a mild anterior uveitis to a fulminant endophthalmitis. Typically, the inflammation is unilateral and involves only the traumatized eye.
• The most important clinical signs of lens-induced uveitis are lid swelling, perilimbal or diffuse injection, corneal haze, keratic precipitates (nongranulomatous or mutton fat), cells and flare, fibrin in the anterior chamber (occasionally), peripheral anterior synechiae, posterior synechiae, pupillary membrane, and iris nodules.
• In the posterior segment, lens fragments, inflammatory cells, traction bands in the vitreous, retinal edema, inflammatory cuffing of blood vessels, cystoid macular edema, and epiretinal membrane formation can be observed.
• If untreated, lens-induced uveitis/phacoanaphylactic endophthalmitis may result in chronic cystoid macular edema, cyclitic membrane formation, tractional retinal detachment, and phthisis bulbi.

Causes

Phacoanaphylactic endophthalmitis/lens-induced uveitis is usually the result of traumatic or surgical disruption of the lens capsule and liberation of lens proteins into the aqueous or into the vitreous cavity. Posterior capsular rupture during phacoemulsification is the most common cause of posterior displacement of lens fragments. This complication is more common in patients with pseudoexfoliation syndrome, zonular dehiscence, a small pupil, friable iris, and hard nuclei or hypermature cataracts.

Penetrating injury of the globe may result in severe lens-induced uveitis. The uveitis may remain undiagnosed clinically because of hyphema, decreased corneal clarity, and inflammation related to the trauma. A small punctured perforation site may remain unnoticed initially (see Images 4-6), and severe inflammation and cataract will be present 1 week later.

Early and total removal of the lens material may prevent trauma-related phacoanaphylaxis and should be performed if the lens capsule is disrupted and a high probability of cataract exists.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Phacoanaphylactic endophthalmitis or lens-induced uveitis may be difficult or impossible to distinguish from other causes of inflammation based on any one clinical sign, but the clinical setting of retained lens material after cataract surgery usually permits the ophthalmologist to make the correct diagnosis. Similarly, rupture of the lens capsule following trauma also points to a lens-induced inflammation. If the eye is injured severely, requiring enucleation, the presence of phacoanaphylaxis often is masked. According to a study by Thatch and Marak, from 144 histologically verified cases of phacoanaphylactic endophthalmitis, in only 6 cases was the diagnosis correct clinically before enucleation.

Posttraumatic endophthalmitis

Endophthalmitis occurs following 2-7% of penetrating injuries. The incidence is higher in association with intraocular foreign bodies, particularly vegetable matter, while the incidence is lower with hot metallic projectiles. Posttraumatic endophthalmitis can progress rapidly. Clinical signs often include marked inflammation with fibrin, hypopyon, and retinal phlebitis. In general, the larger and more contaminated the injury, the more likely endophthalmitis will develop. Anterior chamber tap and vitreous tap should be performed, and intravitreal antibiotic injections should be administered.

Sterile (aseptic) endophthalmitis

Postoperative inflammation occurring in the absence of infection may be acute or chronic and mild to moderately severe. The onset of aseptic endophthalmitis is usually 3-4 days after surgery. Exceptionally, sterile endophthalmitis may occur weeks or months after intraocular surgery, as with late rupture of the anterior hyaloid membrane and vitreous adhesion to the wound in aphakic patients, degradation of implant materials, withdrawal of topical steroid therapy, or dislocation of an intraocular lens (IOL). It can present with hypopyon and cloudy vitreous, but usually no corneal edema, chemosis, or lid swelling is present. Unlike bacterial infections, aseptic endophthalmitis is not severely and progressively painful. Secondary aseptic endophthalmitis often is related to toxic foreign materials inoculated or implanted into the eye at the time of intraocular surgery.

Sympathetic ophthalmia

Clinically, sympathetic ophthalmia presents as a rare bilateral uveitis with an insidious onset and a progressive course. It almost invariably follows a penetrating wound involving uveal tissue produced by either ocular trauma or intraocular surgery. Sympathetic ophthalmia also may occur with laser ciliary ablation procedures, particularly direct contact lasers. Involvement of the noninjured (nonoperated) eye in this disease makes the clinical diagnosis somewhat more straightforward.

The interesting association between phacoanaphylactic endophthalmitis and sympathetic ophthalmia is based upon histopathologic studies. Easom and Zimmerman reviewed 400 cases of sympathetic ophthalmia from the Armed Forces Institute of Pathology and found 7 pairs of eyes with sympathetic ophthalmia. Among them, 2 of the 7 inciting eyes and 6 of the 7 sympathizing eyes demonstrated the classic histopathologic appearance of phacoanaphylactic endophthalmitis instead of sympathetic ophthalmia.

The association of phacoanaphylactic endophthalmitis in sympathetic ophthalmia may be caused by secondary alteration of the lens capsule in sympathetic ophthalmia, or the 2 diseases may be synergistic. One differentiating feature may be the choroidal thickening observed in sympathetic ophthalmia on ultrasound because only minimal choroidal inflammation and thickening occur, even in severe forms of phacoanaphylactic endophthalmitis.

Phacolytic glaucoma

The leakage of lens proteins from mature and hypermature cataracts characterize phacolytic glaucoma. This leakage often is associated with pain, light sensitivity, and marked anterior chamber reaction. The trabecular meshwork becomes blocked by macrophages and high molecular weight proteins, and then increased intraocular pressure develops. Definitive treatment requires cataract surgery.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Aqueous paracentesis in subtle or early cases may reveal inflammatory cells and particulate lens proteins without bacteria. This procedure is performed more efficiently at the time of anterior chamber washout and vitrectomy to remove the inciting lenticular antigens. In cases of suspected bacterial endophthalmitis, intraoperative aqueous and vitreous specimens may establish the diagnosis of phacoanaphylaxis in the absence of positive cultures.

Imaging Studies

• If the media opacity prevents an appropriate fundus examination, echography with A-scan and B-scan may be helpful when evaluating the posterior pole.
• • Suspicion for acute endophthalmitis, intraocular foreign body, dropped lens nucleus, thickening of the choroid, retinal detachment, and choroidal effusion are all indications for echography if the anterior segment changes hinder examination of the posterior segment.
  • The shape, position, and thickness of the traumatized lens; the presence of focal echogenic areas; and, sometimes, even the entrance and exit wounds are recognizable by ultrasound. It is clinically important to diagnose the isolated rupture of the posterior capsule of the lens by echography. Such ruptures are characterized by the irregular extension of the highly reflective posterior capsule toward the vitreous with significantly increased thickness of the lens.
• Ultrasound biomicroscopy (UBM) may have an important role in the evaluation of lens-induced uveitis after extracapsular cataract extraction, revealing hidden lens particles in the posterior chamber causing inflammation as well as lens-particles creating secondary glaucoma.

Histologic Findings

Histopathology of phacoanaphylactic endophthalmitis is characterized by a zonal granulomatous inflammatory reaction consisting of polymorphonuclear neutrophils, numerous epithelioid cells, and occasional giant cells. The inflammatory reaction is around the lens material or lens capsule (see Images 1-3). Associated cells include eosinophils, plasma cells, and histiocytes containing phagocytized lens material.

Minimal histopathologic diagnostic criteria include neutrophil-associated lens damage accompanied by a granulomatous response associated with the lens material. A paucity of neutrophils may be present in late cases. Isolated giant cells without neutrophils and associated lens damage may create difficulty in distinguishing phacoanaphylactic endophthalmitis from a foreign body granuloma since lens material or the Descemet membrane may induce giant cells.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Treatment of phacoanaphylaxis may be medical or surgical. Medical therapy of phacoanaphylactic uveitis includes topical corticosteroids and may include cycloplegics and medication for elevated intraocular pressure as needed. Treatment should be tailored to the individual patient and adjusted according to response. Patient age, immune status, and tolerance for adverse effects always must be taken into account.

• Cycloplegics: Topical cycloplegics break or prevent the formation of posterior synechiae, stabilize the blood-aqueous barrier leading to reduced leakage of plasma proteins, increase uveoscleral outflow, and provide mild relief of ciliary spasm pain. The stronger the inflammatory reaction, the more frequently applied or stronger the cycloplegic.
• Corticosteroids: Corticosteroids block the formation of arachidonic acid from cell membrane precursors by inhibiting the action of phospholipase-A2, cyclooxygenase, and lipoxygenase. Thus, arachidonic acid is the premier precursor of potent inflammatory mediators, such as prostaglandins, thromboxane, and leukotrienes. Corticosteroids frequently are used in uveitis therapy. Topical steroid drops are given in dosages ranging from once daily to hourly. They also can be given in an ointment form. Periocular corticosteroids generally are given as depot-steroid injections when a more prolonged effect is needed or when a patient is noncompliant or poorly responsive to topical administration.
• Intraocular pressure–lowering agents: When phacoanaphylaxis is associated with high intraocular pressure (see Image 8), aqueous suppressants are indicated. Beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors are used to lower the pressure.

Surgical Care

If persistent or uncontrolled inflammation or elevated intraocular pressure is not responsive to medical therapy or if such a large amount of exposed lens material is present that medical therapy is likely to fail, then surgical removal of the exposed lens material is indicated (see Image 7). The most common situation leading to this is posterior capsular rupture with the loss of lens fragments into the vitreous cavity during phacoemulsification (see Images 9-11). Removal of retained lens fragments by pars plana vitrectomy generally restores good visual function and reverses many complications in these patients.

Surgical removal of retained lens material may be necessary depending upon the degree of inflammation, the size of the retained lens particle, and the presence of increased intraocular pressure. Observation is indicated when the lens fragments are small and the inflammation can be controlled.

Retained lens fragments that are larger than one third to one half of the total cataract usually (but not always) require surgical removal. Several studies demonstrate no advantage to early surgery; therefore, the cataract surgeon may treat patients with retained lens fragments conservatively, and then refer the patient to a vitrectomy surgeon after an appropriate period of observation and medical therapy, unless the patient develops retinal detachment, highly elevated intraocular pressure, or some other condition in which posterior segment surgery is indicated more urgently.

• Various techniques have been reported for use by the cataract surgeon at the time of lens fragment loss. However, no apparent advantage exists for immediate removal of retained lens fragments, and such attempts are to be discouraged.
• • A complete limbal vitrectomy should be performed before any lens placement, and the absence of vitreous to the wound or other anterior structures should be confirmed at the time of wound closure. The recommendation from most retina surgeons is to place the IOL in the posterior chamber if there is adequate capsular support and to place anterior chamber lenses if there is inadequate capsular support at the time of the cataract surgery. If the eye is left aphakic at the time of the cataract surgery, secondary IOL insertion is possible at the time of pars plana vitrectomy. Sutured IOL with transscleral fixation may increase the risk of retinal detachment, endophthalmitis, and cystoid macular edema.
  • Kim suggests that the final visual acuity is probably more dependent on the extent of manipulations during the initial cataract surgery than the type of IOL placed or subsequent surgery.
  • Borne et al found perfluorocarbon liquids not to be protective against poor visual outcome. They reported no statistically significant retinal detachment rates in eyes where perfluorocarbon liquid was used compared with eyes in which only vitrectomy was performed to remove retained lens fragments. However, the study conducted by Ross found that patients with retained lens fragments in whom posterior chamber lenses were implanted had a better outcome than patients with anterior chamber lenses, and both groups of pseudophakic patients fared better than aphakic patients. Other studies have failed to find a correlation between IOL placement, type of IOL placed (anterior or posterior chamber IOL), and final visual outcome.
• Surgical outcomes
• • The final visual acuity after vitrectomy for retained lens fragments was 20/40 or better in 60-70% of patients and worse than 20/200 in 10-15% of patients in 2 large retrospective studies.
  • Postoperative complications related to vitrectomy include corneal edema, glaucoma, persistent uveitis, cystoid macular edema, retinal detachment, and endophthalmitis. The same complications are associated with complicated cataract surgery and may coexist before and after pars plana vitrectomy.
  • Retinal detachment is the major cause of a poor visual outcome in the management of retained lens fragments. The frequency of retinal detachment is higher in eyes in which ultrasonic phacofragmentation was used (24%) compared to the eyes in which it was not used (12%), although the difference is not statistically significant. The cumulative incidence of retinal detachment is 15-17% when large series of vitrectomy for retained lens fragment are analyzed.

Activity

In the postoperative period of complicated cataract surgery or pars plana vitrectomy, patients are instructed not to bend over, to avoid extreme physical activities, and to protect the operated eye (eg, glasses, Fox-shield at night) for a minimum of 2 weeks.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. See Medical Care.

Drug Category: Cycloplegics

Cyclopentolate, atropine sulfate, homatropine, and scopolamine break or prevent formation of posterior synechiae; stabilize the blood-aqueous barrier, leading to reduced leakage of plasma proteins; increase uveoscleral outflow; and provide mild relief of ciliary spasm pain. The stronger the inflammatory reaction, the more frequently applied or stronger the cycloplegic.

Drug Category: Corticosteroids

Block formation of arachidonic acid from cell membrane precursors by inhibiting action of phospholipase-A2. Corticosteroids frequently are used in uveitis therapy. Topical corticosteroids are given in dosages ranging from once daily to hourly. They also can be given in an ointment form. Periocular corticosteroids generally are given as depot-steroid injections when a more prolonged effect is needed or when a patient is noncompliant or poorly responsive to topical administration.

Drug Category: Nonsteroidal anti-inflammatory agents (NSAIDs)

Inhibit cyclooxygenase pathway that controls prostaglandin biosynthesis. NSAIDs have both topical analgesic and anti-inflammatory effects. Although NSAIDs currently do not have a significant role in uveitis therapy beyond the treatment of macular edema, they may have a synergistic effect with topical corticosteroids, and, because of minimal adverse effects, they often are used in cases of intraocular inflammation.

Drug Category: Beta-adrenergic blocking agents

Decrease production of aqueous humor by the ciliary epithelium, resulting in decreased intraocular pressure. Beta-blockers reduce aqueous formation by 24-48%.

Drug Category: Alpha2-adrenergic agonists

Potent inhibitors of aqueous production, reducing it by 35-40%.

Drug Category: Carbonic anhydrase inhibitors

These agents are nonbacteriostatic sulfonamides that inhibit enzyme carbonic anhydrase (eg, topical dorzolamide, brinzolamide, systemic methazolamide, acetazolamide). This action reduces the rate of aqueous humor production, resulting in decreased intraocular pressure.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Follow-up care of patients with phacoanaphylaxis or retained lens material should be scheduled according to the severity of symptoms and the preoperative or postoperative condition of the patient.

Complications

• Cystoid macular edema: The incidence of cystoid macular edema after complicated cataract surgery with retained lens material has been reported to be approximately 7%.
• Secondary glaucoma
• • The incidence of secondary glaucoma related to retained lens fragment was 30% in one study and 52% in another study.
  • Leakage of lens proteins through the injured lens capsule with or without leakage of serum proteins from uveal blood vessels in lens-induced uveitis may block the trabecular outflow causing secondary glaucoma.
  • Trabecular meshwork obstruction may occur with the accumulation of white blood cells (macrophages and activated T lymphocytes) or their aggregations. These may cause peripheral anterior synechiae and subsequent closed-angle glaucoma.
  • Obstruction may arise from inflammatory debris (eg, proteins, fibrin, high molecular weight proteins) and from lens particles. These proteins increase the aqueous viscosity, which may contribute to increased intraocular pressure.
• Retinal detachment
• • The incidence of retinal detachment after cataract surgery complicated by retained lens material is 7-11%. This is not a result of damage to the retina from sharp lens fragments or the inflammation associated with phacoanaphylaxis but is related to complications of the cataract surgery, such as vitreous loss.
  • Vigorous attempts to retrieve the lens fragments from the vitreous cavity via an anterior segment incision during phacoemulsification have been associated with giant retinal tears and poor prognosis.

Prognosis

• Prognosis of phacoanaphylaxis without surgical treatment is dismal. With appropriate surgical and medical treatment, the prognosis of retained lens material is much more favorable, especially with today's state-of-the-art surgical techniques.
• • Several series reported visual acuities of 20/40 or better in 60-82% of patients with retained lens material after vitrectomy.
  • Postoperative complications related to vitrectomy may be difficult to distinguish from complications related to the initial cataract surgery. (See Surgical Care.)
  • The prognosis in trauma cases is highly correlated to the extent of trauma and the visual acuity at the time of initial evaluation.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• The eye care specialist should emphasize the need for prompt cataract removal in mature and hypermature cataracts.
• With extracapsular and phacoemulsification cataract removal, retained lens material may cause inflammation.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Gross photomicrograph for eye enucleated with penetrating injury
	View Full Size Image
Media type:  Photo

Media file 2:  Gross photomicrograph for eye enucleated with penetrating injury. Note marked inflammatory reaction consisting of polymorphonuclear cells around lens capsule and lens fibers (hematoxylin and eosin X100).
	View Full Size Image
Media type:  Photo

Media file 3:  Low (X25) photomicrograph of phacoanaphylactic reaction to lens protein in eye enucleated with penetrating injury. Note polymorphonuclear leucocytes around lens protein (hematoxylin and eosin).
	View Full Size Image
Media type:  Photo

Media file 4:  High (X50) photomicrograph of phacoanaphylactic reaction to lens protein in eye enucleated with penetrating injury. Note polymorphonuclear leucocytes around lens protein (hematoxylin and eosin).
	View Full Size Image
Media type:  Photo

Media file 5:  Phacoanaphylactic reaction to penetrating injury of lens. This patient was a 25-year-old woman whose eye was penetrated with a 27-gauge needle during an attempt to anesthetize the eyelid for chalazion removal. One week later, a marked uveitis was present. Notice perforation site and posterior synechiae.
	View Full Size Image
Media type:  Photo

Media file 6:  Same patient as in Image 5. Notice cortical cataract at perforation site.
	View Full Size Image
Media type:  Photo

Media file 7:  Typical clinical picture of retained lens material following cataract surgery. White cortical material is easily visible in the pupillary space.
	View Full Size Image
Media type:  Photo

Media file 8:  Patient with persistently elevated intraocular pressure after cataract surgery was found to have retained lens material and low-grade inflammation. Eye is white and quiet with anterior chamber lens.
	View Full Size Image
Media type:  Photo

Media file 9:  Patient with persistently elevated intraocular pressure after cataract surgery was found to have retained lens material and low-grade inflammation. Retained lens material is visible in retroillumination on downgaze.
	View Full Size Image
Media type:  Photo

Media file 10:  Typical appearance of retained lens fragments in posterior vitreous cavity. Lens material is a whitish substance that obscures fundus details.
	View Full Size Image
Media type:  Photo

Media file 11:  Another view of a retained lens fragment, noted inferiorly.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Aaberg TM Jr, Rubsamen PE, Flynn HW Jr, et al. Giant retinal tear as a complication of attempted removal of intravitreal lens fragments during cataract surgery. Am J Ophthalmol. Aug 1997;124(2):222-6. [Medline].
• Allen JC. Sympathetic uveitis and phacoanaphylaxis. Am J Ophthalmol. Feb 1967;63(2):280-3. [Medline].
• Alward WL, Byrne SF, Hughes JR, Hodapp EA. Dislocated lens nuclei simulating choroidal melanomas. Arch Ophthalmol. Oct 1989;107(10):1463-4. [Medline].
• Apple DJ, Mamalis N, Steinmetz RL, et al. Phacoanaphylactic endophthalmitis associated with extracapsular cataract extraction and posterior chamber intraocular lens. Arch Ophthalmol. Oct 1984;102(10):1528-32. [Medline].
• Besen G, Freeman WR. Intraoperative recognition of retinal vasculitis in a patient with early lens-induced uveitis. Ophthalmic Surg Lasers. Jan 1997;28(1):67-8. [Medline].
• Bloch-Michel E, Nussenblatt RB. International Uveitis Study Group recommendations for the evaluation of intraocular inflammatory disease. Am J Ophthalmol. Feb 15 1987;103(2):234-5. [Medline].
• Blodi BA, Flynn HW Jr, Blodi CF, et al. Retained nuclei after cataract surgery. Ophthalmology. Jan 1992;99(1):41-4. [Medline].
• Blodi FC. Sympathetic uveitis as an allergic phenomenon: with a study in association with phacoanaphylactic uveitis and a report on the pathological findings in sympathizing eyes. Trans Am Acad Ophthal Otolaryng. 1959;63:642-649.
• Borne MJ, Tasman W, Regillo C, et al. Outcomes of vitrectomy for retained lens fragments. Ophthalmology. Jun 1996;103(6):971-6. [Medline].
• Bourke RD, Gray PJ, Rosen PH, Cooling RJ. Retinal detachment complicating scleral-sutured posterior chamber intraocular lens surgery. Eye. 1996;10 ( Pt 4):501-8. [Medline].
• Brinkman CJ, Broekhuyse RM. Cell mediated immunity in relation to cataract and cataract surgery. Br J Ophthalmol. May 1979;63(5):301-5. [Medline].
• Burky EL, Woods AC. Lens extract: its preparation and clinical use. Arch Ophthalmol. 1931;6:548-553.
• Chan CC. Relationship between sympathetic ophthalmia, phacoanaphylactic endophthalmitis, and Vogt-Koyanagi-Harada disease. Ophthalmology. May 1988;95(5):619-24. [Medline].
• Chishti M, Henkind P. Spontaneous rupture of anterior lens capsule (phacoanaphylactic endophthalmitis). Am J Ophthalmol. Feb 1970;69(2):264-70. [Medline].
• Croxatto JO, Rao NA, McLean IW, Marak GE. Atypical histopathologic features in sympathetic ophthalmia. A study of a hundred cases. Int Ophthalmol. Feb 1982;4(3):129-35. [Medline].
• Easom H, Zimmerman LE. Sympathetic ophthalmia and bilateral phacoanaphylaxis. A clinicopathologic correlation of the sympathogenic and sympathizing eyes. Arch Ophthalmol. Jul 1964;72:9-15. [Medline].
• Easom HA, Zimmerman LE. Sympathetic ophthalmia and bilateral phacoanaphylaxis. A clinicopathological correlation of the sympathogenic and sympathizing eyes. Arch Ophthalmol. 1964;72:9-15.
• Ellant JP, Obstbaum SA. Lens-induced glaucoma. Doc Ophthalmol. 1992;81(3):317-38. [Medline].
• Emery JM, Wilhelmus KA, Rosenberg S. Complications of phacoemulsification. Ophthalmology. Feb 1978;85(2):141-50. [Medline].
• Endophthalmitis Vitrectomy Study Group. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Endophthalmitis Vitrectomy Study Group. Arch Ophthalmol. Dec 1995;113(12):1479-96. [Medline].
• Epstein DL. Diagnosis and management of lens-induced glaucoma. Ophthalmology. Mar 1982;89(3):227-30. [Medline].
• Epstein E. Suture problems. J Cataract Refract Surg. Jan 1989;15(1):116. [Medline].
• Fastenberg DM, Schwartz PL, Shakin JL, Golub BM. Management of dislocated nuclear fragments after phacoemulsification. Am J Ophthalmol. Nov 15 1991;112(5):535-9. [Medline].
• Fine HI. Small incision cataract surgery. In: Yanoff M, Duker JS. Ophthalmology. 1st ed. Mosby Inc;1999:23.1-10.
• Fisher D. Glaucoma associated with uveitis (Inflammatory glaucoma). In: Eid TM, Spaeth GL. The Glaucomas: Concepts and Fundamentals. Lippincott Williams & Wilkins;2000:190-198.
• Friedlander MH. Allergy and Immunology of the Eye. Lippincott-Raven Publishers;1979:24-203.
• Gass JD, Norton EW. Follow-up study of cystoid macular edema following cataract extraction. Trans Am Acad Ophthalmol Otolaryngol. Jul-Aug 1969;73(4):665-82. [Medline].
• Gifford SR. Allergic and toxic properties of lens protein. JAMA. 1925;85:351-356.
• Gilliland GD, Hutton WL, Fuller DG. Retained intravitreal lens fragments after cataract surgery. Ophthalmology. Aug 1992;99(8):1263-7; discussion 1268-9. [Medline].
• Goodner EK. Experimental lens-induced uveitis in rabbits. In: Maumenee AE, Silverstein AM, ed. Immunopathology of Uveitis. Lippincott Williams & Wilkins;1964:233-242.
• Greve MD, Peyman GA, Mehta NJ, Millsap CM. Use of perfluoroperhydrophenanthrene in the management of posteriorly dislocated crystalline and intraocular lenses. Ophthalmic Surg. Sep 1993;24(9):593-7. [Medline].
• Habil I, Cohen E, Karshai I. Spontaneous involution of autologous lenses and phacoanaphylaxis reaction in Stickler syndrome. Br J Ophthalmol. Nov 2005;89(11):1532-3. [Medline].
• Halbert SP, Manski W. Biological aspects of autoimmune reactions in the lens. Invest Ophthal. 1965;4:516-530.
• Hektoen L, Schulhof K. Further observations on lens precipitins. Antigenic properties of alpha and beta crystallins. J Infect Dis. 1924;34:433-439.
• Inomata H, Yoshikawa H, Rao NA. Phacoanaphylaxis in Behcet's disease: a clinicopathologic and immunohistochemical study. Ophthalmology. Oct 2003;110(10):1942-5. [Medline].
• Irvine SR, Irvine AR Jr. Lens-induced uveitis and glaucoma: Endophthalmitis phacoanaphylactica. Am J Ophthalmol. 1952;35:177.
• Ishikawa Y, Kawata K. Three cases of endophthalmitis phacoanaphylactica in the fellow eye after extracapsular lens extraction. Folia Ophthalmol Jpn. 1977;28:1260-1265.
• Jaffe NS. Cataract Surgery & Its Complications. St. Louis:. Mosby Inc;1976:367-370.
• Kida H. Experimental endophthalmitis phacoanaphylactica in rabbits sensitized with the purified bovine alpha-crystallin. Folia Ophthalmol Jpn. 1961;12:304-311.
• Kim JE, Flynn HW Jr, Smiddy WE, et al. Retained lens fragments after phacoemulsification. Ophthalmology. Nov 1994;101(11):1827-32. [Medline].
• Kincses E, Szabo G. Human and cellular immune response after injury of the lens . In: Ocular Immune Responses: Proceedings of the International Symposium on Immunology & Immunopathology of the Eye. Strasbourg:. S Karger AG Basel Publisher;1974:16.
• Kraff MC, Sanders DR, Lieberman HL, et al. Membrane formation after implantation of polyvinyl alcohol-coated intraocular lenses. J Am Intraocul Implant Soc. Apr 1980;6(2):129-36. [Medline].
• Kronenthal RL. Nylon in the anterior chamber. Ophthalmology. Sep 1981;88(9):965-7. [Medline].
• Lambrou FH Jr, Stewart MW. Management of dislocated lens fragments during phacoemulsification. Ophthalmology. Aug 1992;99(8):1260-2; discussion 1268-9. [Medline].
• Leaming DV. Practice styles and preferences of ASCRS members--1994 survey. J Cataract Refract Surg. Jul 1995;21(4):378-85. [Medline].
• Little J, Langman J. Lens antigens in the intraocular tissues of the human eye. Arch Ophthal. 1964;72:820-825.
• Lubin JR, Albert DM, Weinstein M. Sixty-five years of sympathetic ophthalmia. A clinicopathologic review of 105 cases (1913--1978). Ophthalmology. Feb 1980;87(2):109-21. [Medline].
• Luntz MH, Wright R. Lens-induced uveitis. Exp Eye Res. 1962;1:317-323.
• Maisel H, Goodman M. Analysis of mammalian lens proteins by electrophoresis. Arch Ophthal. 1964;71:671-675.
• Marak GE Jr. Phacoanaphylactic endophthalmitis [published erratum appears in Surv Ophthalmol 1992 May-Jun;36(6):454]. Surv Ophthalmol. Mar-Apr 1992;36(5):325-39. [Medline].
• McCluskey P, Harrisberg B. Long-term results using scleral-fixated posterior chamber intraocular lenses. J Cataract Refract Surg. Jan 1994;20(1):34-9. [Medline].
• McMahon MS, Weiss JS, Riedel KG. Clinically unsuspected phacoanaphylaxis after extracapsular cataract extraction with intraocular lens implantation. Br J Ophthalmol. Nov 1985;69(11):836-40. [Medline].
• Mehta PD, Cooper SN, Rao SS. Identification of species -specific and organ-specific antigens in lens proteins. Exp Eye Res. 1964;3:192-199.
• Meltzer DW. Sterile hypopyon following intraocular lens surgery. Arch Ophthalmol. Jan 1980;98(1):100-4. [Medline].
• Muccioli C, Belfort R Jr. Cataract surgery in patients with uveitis. Int Ophthalmol Clin. Spring 2000;40(2):163-73. [Medline].
• Muller H. Phacolytic glaucoma and phacogenic ophthalmia (lens-induced uveitis). Trans Ophthal. Soc. UK. 1963;83:689-704.
• Pavlin CJ, Harasiewicz K, Sherar MD, Foster FS. Clinical use of ultrasound biomicroscopy. Ophthalmology. Mar 1991;98(3):287-95. [Medline].
• Perlman EM, Albert DM. Clinically unsuspected phacoanaphylaxis after ocular trauma. Arch Ophthalmol. Feb 1977;95(2):244-6. [Medline].
• Perlman EM, Albert DM. Clinically unsuspected phacoanaphylaxis after ocular trauma. Arch Ophthalmol. Feb 1977;95(2):244-6. [Medline].
• Rahi AH, Garner A. Immunopathology of the Eye. Oxford, England:. Blackwell Scientific Publications;1976.
• Ritch R. Exfoliation syndrome and exfoliative glaucoma. In: Eid TM, Spaeth GL. Glaucomas: Concepts and Fundamentals. Lippincott Williams & Wilkins;2000:114-120.
• Sampaolesi R. Three-dimensional scan using a single transducer and image construction. In: Tomita M, Sugata Y, Yamamoto Y, eds. Ultrasonography in Ophthalmology 12, Documenta Ophthalmologica Proceedings. Kluwer Academic Publishers;1990:455-460.
• Schechter RJ. Glass-slide vitrectomy for use by the cataract surgeon. Am J Ophthalmol. Jul 15 1991;112(1):100. [Medline].
• Schubert HD. Postsurgical hypotony: relationship to fistulization, inflammation, chorioretinal lesions, and the vitreous. Surv Ophthalmol. Sep-Oct 1996;41(2):97-125. [Medline].
• Sheppard JD, Nozik RA. Practical Diagnostic Approach to Uveitis. Duane TA, Jaeger EW eds: Clinical Ophthalmology, JB Lippincott, Philadelphia. 1989;4, chapter 33.
• Sheppard JD. Sympathetic Ophthalmia. Beatty RL, ed.: Seminars in Ophthalmology, JB Lippincott, Philadelphia. 1994.
• Smiddy WE, Flynn HW. Management of retained lens fragments and dislocated posterior chamber intraocular lenses. In: Albert DM, Jakobiec FA. Principles and Practice of Ophthalmology. WB Saunders Co;2000:2485-2494.
• Speaker MG, Smolin G, Menikoff JA, Friedlaender MH, eds. Postoperative endophthalmitis: Pathogenesis, prophylaxis and management. In: International Ophthalmology Clinics. Vol 33. 1993:51-70.
• Stark WJ, Rosenblum P, Maumenee AE, Cowan CL. Postoperative inflammatory reactions to intraocular lense sterilized with ethylene-oxide. Ophthalmology. May 1980;87(5):385-9. [Medline].
• Thach AB, Marak GE Jr, McLean IW, Green WR. Phacoanaphylactic endophthalmitis: a clinicopathologic review. Int Ophthalmol. Jul 1991;15(4):271-9. [Medline].
• Thompson JT, Parver LM, Enger CL, et al. Infectious endophthalmitis after penetrating injuries with retained intraocular foreign bodies. National Eye Trauma System. Ophthalmology. Oct 1993;100(10):1468-74. [Medline].
• Toris CB, Pederson JE. Aqueous humor dynamics in experimental iridocyclitis. Invest Ophthalmol Vis Sci. Mar 1987;28(3):477-81. [Medline].
• Truhlsen SM. Approaching nucleus slippage. Arch Ophthalmol. May 1991;109(5):627. [Medline].
• Uhlenhuth P. Zur Lehre von der Unterscheidung verschiedener Eiweissarten mit Hilfe spezifischer Sera. In: Festschrift zum Geburstag Robert Koch. Gustav Fischer Verlag;1903:49-74.
• Verhoeff FH, Lemoine AN. Endophthalmitis phacoanaphylactica. Am J Ophthalmol. 1922;5:737-745.
• Vilar NF, Flynn HW Jr, Smiddy WE, et al. Removal of retained lens fragments after phacoemulsification reverses secondary glaucoma and restores visual acuity. Ophthalmology. May 1997;104(5):787-91; discussion 791-2. [Medline].
• Volcker HE, Naumann GO. Morphology of uveal and retinal edemas in acute and persisting hypotony. Mod Probl Ophthalmol. 1979;20:34-41. [Medline].
• Weinstein GW, Charlton JF, Esmer E. The "lost lens": a new surgical technique using the Machemer lens. Ophthalmic Surg. Mar-Apr 1995;26(2):156-9. [Medline].
• Winward KE, Pflugfelder SC, Flynn HW Jr, et al. Postoperative Propionibacterium endophthalmitis. Treatment strategies and long-term results. Ophthalmology. Apr 1993;100(4):447-51. [Medline].
• Woods AC. An adventure in ophthalmic literature: Manuel Straub and the tradition of toxicity in lens protein. Am J Ophthalmol. 1959;48:463-472.
• Zimmerman LE. Lens induced inflammation in human eyes. In: Maumenee AE, Silverstein AM, eds. Immunopathology of Uveitis. Lippincott Williams & Wilkins;1964:221-232.

Article Last Updated: Sep 25, 2006