International Ophthalmology 15: 271-279, 1991.

9 1991 Kluwer Academic Publishers. Printed in the Netherlands.

Phacoanaphylactic endophthalmitis: a clinicopathologic review

Allen B. Thach, 1 George E. Marak Jr.,2 Ian W. McLean 3 & W. Richard Green 4
1Walter Reed Army Medical Center, Washington, D.C. 20307; 22059 Huntington Ave. # P14, Alexandria,
VA 22303; 3Armed Forces Institute Pathology, Washington, D.C. 20307; 4Eye Pathology Laboratory,
The Johns Hopkins Hospital, Baltimore, MD 21205, USA

Accepted 22 November 1990

Key words: Arthus reaction, immune complex-mediated reaction, phacoanaphylactic endophthalmitis, lens-
induced uveitis, uveitis

Abstract

Lens-induced uveitis or phacoanaphylactic endophthalmitis (PE) is a chronic endophthalmitis with a zonal

granulomatous inflammation surrounding a ruptured lens. One hundred forty four cases of PE were
retrospectively evaluated clinically and histopathologically. The disease was not well recognized clinically as
only six of the cases were given the clinical diagnosis of PE. Most cases (80%) occurred after trauma, surgical
or non-surgical. The time after injury varied from two days to fifty nine years. Of those individuals less than
55 years of age who had no history of trauma, 29% were noted by clinical history to have microphthalmia.
Although classically the inflammation of PE has been described as being confined to the anterior aspect of
the eye, the choroid was involved with an inflammatory reaction in 76% of the cases.

Introduction many years. A number of careful studies providing

Endophthalmitis phacoanaphylactica was first de-
scribed by Straub in 1919 [1] and later elaborated by
Verhoeff and Lemoine in 1922 [2]. They described
a severe uveitis that developed 1 to 14 days after
leakage of lens material into the anterior chamber.
At that time the term 'anaphylactic' described a
sudden onset of inflammation. For many years it
was mistakenly believed that phacoanaphylactic
endophthalmitis (PE) was analogous to the rejec-
tion of a foreign tissue graft. Disease was proposed
to develop when sequestered lens protein was ex-
posed to immunologic surveillance by disruption of
the lens capsule. This 'idee fixe' so dominated
thinking about PE that it misdirected work for
contradictory evidence were ignored [3].
PE is not a cell mediated rejection of foreign
tissue. Experimental studies have shown that PE
represents an Arthus-type immune complex medi-
ated response to exposed lens material which has
been released by trauma or degeneration [4, 5].
The capacity to develop experimental disease can
be passively transferred by hyperimmune serum [6,
7]. It has been proposed that lens-induced endoph-
thalmitis results from the breakdown of T-cell tol-
erance, normally maintained by small amounts of
circulating lens protein [8-10]. Bacterial lipopoly-
saccharide is mitogenic for B-lymphocytes and may
be used to bypass the need for tolerant T-lympho-
cytes [11]. If antigen-recognizing B-lymphocytes

The opinions and assertations contained herein are the private views of the authors and are not to be construed as official or reflecting
the views of the Department of the Army or the Department of Defense.
272 A.B. Thach et al.
are present, they may be stimulated by lipopoly-
saccharide, introduced by wound contamination,
to produce disease after lens injury without presen-
sitization [12].
In those cases with infection the granulomatous
response to the lens is at a site distinct from the
major focus of the infection. Infectious agents such
as Propionibacterium acnes may induce granulo-
matous inflammation [13] and intraocular implants
may induce a PE-like picture that has been termed
pseudo-PE [14]. The observation of a PE reaction
in conjunction with degenerating lens material par-
ticularly at a site remote from the focus of the
infection or implant may be of value in distinguish-
ing PE from the direct response to infection or an
intraocular lens implant.
Clinically PE has been described in patients with
decreased vision and inflammation that has varied
from a mild iritis to a fulminant endophthalmitis.
The inflammation may develop insidiously or
acutely with congestion, a hazy cornea and white
keratic precipitates. Typically the onset has been
described as occurring several days to several
months after traumatic or surgical capsular dis-
ruption [2, 15-17]. The inflammation is usually un-
iocular and involves the traumatized eye. Ultra-
sound may be used to detect inflammation cen-
tered around the lens or within the vitreous [18].
The diagnosis of PE may be confirmed by study of
anterior chamber or vitreous aspirate containing
fragments of lens material [19-21]. An association
with sympathetic ophthalmia has been described
[22-27] and this association may sometimes be con-
fused with a bilateral presentation of PE [27, 28].
The classic histologic picture of this disease is a
zonal, granulomatous reaction centered around
the lens or lens remnants. Polymorphonuclear lym-
phocytes are seen at the margin of the disrupted
lens. This is surrounded by a layer of large mono-
nuclear cells including epithelioid cells, macro-
phages and giant cells. The outermost layer is vari-
able in thickness and has granulation tissue heavily
infiltrated by lymphocytes and plasma ceils [29,
30]. The lens capsule is always ruptured. The lens
cortex and nucleus show various degrees of cat-
aractous damage. The adjacent tissues, including
iris, ciliary body and anterior chamber are usually
infiltrated by numerous lymphocytes, plasma cells
and macrophages. It has been noted that the ante-
rior segment is the only part of the eye principally
involved, distinguishing it from such entities as
sympathetic ophthalmia [31].
Treatment of PE involves the surgical removal of
all remaining lens material [2, 17, 32-38]. Addi-
tionally, topical and systemic corticosteroids may
be used to reduce the ocular inflammation.
This study retrospectively reviews the clinical
and histopathologic features of 144 cases of PE,
providing observations on previously unempha-
sized features of this disease.
Materials and methods
Selection of cases. One hundred seventy four cases
of PE, dating from 1970 to 1988, from the files of
the Registry of Ophthalmic Pathology at the
Armed Forces Institute of Pathology and fifty nine
cases from the Eye Pathology Laboratory, Wilmer
Ophthalmological Institution were evaluated. Of
those cases reviewed 144 were included in this
study. Criteria for inclusion were a) availability of
clinical data and b) histopathologic slide demon-
strating granulomatous inflammation around the
lens. Hematoxalin and eosin and Periodic acid
Schiff stained slides were examined. Those slides
with giant cells/epithelioid cells but without any
evidence of acute inflammation were excluded
from the study.
Trauma. The determination as to whether the pa-
tient was subject to ocular trauma was derived from
the history and if there was no history of trauma the
histopathologic specimen was reviewed for evi-
dence of injury (corneal/scleral wound, angle re-
cession, etc.)
Severity of phacoanaphylactic reaction. The sever-
ity of the phacoanaphylactic reaction was consid-
ered mild (Fig. 1) if there were few inflammatory
cells involving the lens only with no evidence of
surrounding tissue involvement. A moderate reac-
tion was based on a moderate to heavy inflammato-
ry reaction around the lens with no involvement of

Fig. 1. Mild phacoanaphylacticendophthalmitis. Note the mini-
mal involvementof surroundingtissue and the mildinflammato-
ry reaction surrounding the lens.
the surrounding tissues or a mild to moderate in-
flammatory reaction around the lens with evidence
of involvement of the surrounding tissues. A reac-
tion was judged to be severe (Fig. 2) if the in-
flammatory reaction around the lens was heavy and
there was evidence of involvement of the surround-
ing tissues.
Bacteria. Fifty five slides were stained by the
Brown and Hopps, Brown and Benn or MacCul-
lum-Goodpasture method. These slides were ex-
amined for the presence of bacteria.
Statistical analysis. The probabilities of the associ-
ations studied were calculated using the Chi-square
distribution functions with Yates continuity correc-
tion for two by two tables. The associations were
considered significant at the P < 0.05 level.
Phacoanaphylactic endophthalmitis 273
Fig. 2. Severephacoanaphylacticreaction with a granulomatous
inflammatory infiltrate surrounding lens fibers.
Results
The cases reported in this series were obtained
from the Armed Forces Institute of Pathology and
the Wilmer Ophthalmological Institution. The re-
sults obtained from both were very similar and will
be reported as cummulative data.
The demographic and clinical characteristics of
the cases in this study are listed in Table 1. The
range of age is quite variable with PE occurring
most often in the fifth to seventh decade. The visual
acuity in every patient, except one, was light per-
ception or worse.
Table 2 summarizes the association of P E and
trauma. As noted, 80% of the patients suffered
some form of surgical or non-surgical trauma. Of
those who did not have a history of trauma 52%
were older than 55 years of age, and onset of PE
was probably related to the development of cat-
274 A . B . Thach et al.

Table 1. Demographic and clinical characteristics. aracts. O f the fourteen patients who were younger
than 55 years of age, four were noted by history to
Age Mean 53
Range 1-89 have microphthalmia and one had a history of ru-
Sex Male 61% bella.
Female 39% All the clinical diagnoses reported (more than
Ocular involvement OD 47% one diagnosis given in some patients) are listed in
OS 52%
Table 3. Of particular interest is that of the 144
ou 1%
Visual Acuity Light perception or better 22% cases studied only six individuals were diagnosed
No light perception 78% with phacoanaphylactic endophthalmitis.
Intra-ocular pressure High (->23) 18%
Normal (10-22) 24% Lens. The lens capsule in every case was found on
Low (-< 9) 58% at least one section to be disrupted. Disruption of
the lens capsule was necessary (either traumatic or
Table 2. Association with trauma. spontaneous rupture) in order that the inflammato-
ry cells reach the lens material. The inflammatory
Trauma 115 (80%) reaction though involving both the cortex and nu-
No trauma 29 (20%) cleus seemed to cause a much slower destruction of
< 55 years old 14 (48%)
->55 years old 15 (52%) the nucleus. In m a n y specimen the cortex was com-
Time after injury pletely destroyed, whereas the nucleus remained
Mean 8 years relatively intact.
Range 2 days-59 years
Within first year 52% I n f l a m m a t o r y reaction. The classic histologic de-
Type of trauma
Surgical 45 (39%) scription of this reaction is a zonal, granulomatous
Non-surgical 65 (57%) inflammation centered around lens material. Cen-
Both 5 (4%) trally the lens tissue is infiltrated by polymorpho-
nuclear leukocytes with an adjacent layer of mono-
nuclear cells to include epithelioid and giant cells.
Table 3. Clinical diagnosis.
Several slides reviewed with the diagnosis of PE
Phthisis 35 were excluded from the study because although
Glaucoma 24 they had epithelioid and giant cells, there was no
Iritis 17 acute inflammation (Fig. 3).
Endophthalmitis 13
Sympathetic ophthal. 13
Tumor 8 Choroidal involvement. Inflammation of the cho-
Phacoanaphylaxis 6 roid was noted in 110 (76%) of the cases reviewed.
Other 29 The cells involved in the choroid were non-granu-
No diagnosis 18 lomatous mononuclear cells. The inflammatory re-
sponse occurred both in the anterior and posterior
Table 4. Choroidal involvement and its relationship to the sever- choroid. Involvement of the choroid related to the
ity of PE inflammation. severity of inflammation (Table 4). The cases of
m o d e r a t e ( P < 0.05) and severe ( P < 0.01) PE
Mild inflammation Choroid involved 14 were m o r e likely to have choroidal involvement
No involvement 13 than those reactions judged to be mild.
Moderate inflammation Choroid involved 60
(e < 0.05)
No involvement 17 Retina. The retina was involved in the inflammato-
Severe inflammation Choroid involved 36 ry reaction in 51% of the cases. In m a n y of the cases
(P < o.ol) the inflammatory reaction in the retina consisted of
No involvement 4 a perivasculitis. The inflammation of the retina did
 Phacoanaphylactic endophthalmitis 275

Fig. 3. A case excluded from this study because of the lack of Fig. 4. Non-granulomatousmononuclearresponse in the poste-
acute inflammatory cells. The presence of the giant cells alone rior choroidin this case of moderate phacoanaphylacticendoph-
does not constitute the diagnosis. thalmitis.

Table 5. Histopathologicdiagnosis. not correlate with the overall severity of inflamma-

Phacoanaphylaxis 144 tion (P < 0.1). The retina was noted to be detached
Retinal detachment 95 in 64% of the cases studied. Detachment of the
Corneal/scleral wound 59 retina was not related to the amount of inflamma-
Optic atrophy 40
tion.
Phthisis bulbi 18
Rubeosis 18
Fib./epith. ingrowth 16 Associated histopathologic diagnoses. Table 5 sum-
Peripheral anterior synechiae 12 marizes the most c o m m o n associated histopath-
Keratopathy 12 ologic diagnoses. As expected with trauma many
Siderosis 9
patients were noted to have a corneal-scleral
Endophthalmitis 7
S.O. 4 wound and/or fibrous or epithelial ingrowth. The
large number of cases with optic atrophy and phthi-
sis bulbi corresponds with the end stage condition
Table 6. Bacterial involvement.
of these eyes. Sympathetic ophthalmia was observ-
No bacteria 53 (95%) ed in four cases.
Bacterial involvement 3 (5%)
Gram positive cocci 2
Bacteria. A total of 56 specimens were stained with
Mixed gram positive organisms 1
a tissue gram stain. Only three of these specimens
276 A.B. Thach etal.
had demonstrable bacterial involvement. Two had
gram positive cocci involvement and one had gram
positive rods and cocci (Table 6).
Discussion
Phacoanaphylactic endopthalmitis (PE) has a vari-
able clinical presentation, making the diagnosis dif-
ficult. On routine exam the condition may be indis-
tinguishable from a granulomatous uveitis or en-
dophthalmitis due to other causes. The varied clin-
ical presentation may explain the low rate of
primary diagnosis in this series. A high index of
suspicion should be present for PE in eyes with lens
material present, granulomatous inflammation and
a history of surgical or non-surgical trauma. It is
important that the clinician differentiates between
PE and phacolytic glaucoma, bacterial endophthal-
mitis, sympathetic ophthalmia, toxic response to
intraocular lens implant and uveitis of other causes.
Phacolytic glaucoma usually presents with in-
creased intraocular pressure, secondary to lens ma-
terial blocking the trabecullar meshwork, macro-
phages engorged with lens material are usually pre-
sent in the angle and the anterior chamber. Keratic
precipitates and posterior synechiae, often present
in PE, are usually absent in phacolytic glaucoma.
Bacterial endophthalmitis usually presents within a
week after surgery or trauma with increasing pain,
hyperemia, chemosis, lid and corneal edema, ante-
rior chamber and vitreous inflammation and a de-
creased retinal reflex. Sympathetic ophthalmia is a
bilateral granulomatous inflammation usually oc-
curring two weeks or more after an injury. Clinical-
ly, the patient presents with a persistant bilateral
uveitis with 'mutton fat' keratic precipitates, iris
and pupillary nodules, posterior synechiae and the
appearance of yellow-white nodules in the periph-
eral fundus. Failure to diagnose PE may result in an
unremitting course of chronic inflammation, lead-
ing to synechiae, retinal detachment, optic atrophy
and phthisis bulbi.
In patients with PE the visual acuity is quite
variable, ranging from 20/30 to no light perception
[1, 17, 18, 32, 34, 36]. The finding of no light per-
ception in 78% of the patients in this study is more
an indication of the end stage clinical state of these
eyes than of the vision to expect in most patients
with PE. If treated at an early stage several reports
note return of useful visual acuity [32, 34].
The intraocular pressure is variable and may pre-
sent as high [1, 2, 34, 39, 40], normal [41] or low
[17]. Patients with high pressures are presumably
the result of posterior synechiae, peripheral ante-
rior synechiae or the obstruction of the trabecullar
meshwork with inflammatory cells. The low pres-
sure is the result of long term inflammation result-
ing in phthisis bulbi. The cases reported in this
study ran the gamut from 0 to 70 mmHg.
The peak incidence of PE in the fifth to seventh
decade of life is probably related to the devel-
opment and surgical removal of catactous lenses as
well as the need for other surgical treatment of
ocular disease rather than an increased incidence of
non-surgical trauma in this age group.
PE is classically reported to occur after surgical
or non-surgical trauma, yet it has been reported to
occur after spontaneous rupture of the lens capsule
[39, 41]. The spontaneous rupture of the anterior
lens capsule previously reported has occurred in
eyes with cataracts and is presumably the result of
increased lenticular volume with an associated cap-
sular weakness. We report 29 cases where there
was no clinical or histopathologic evidence of trau-
ma. Of those 60 years of age and older the capsular
rupture can be imputed to cataractous changes. Of
those individuals less than age 60, 4 of 14 patients in
this group were noted by clinical history to have
microphthalmia and one patient had a history of
rubella. Other studies have noted the presence of
posterior capsular rupture [42] and PE in cases of
PHPV [43]. The association of microphthalmia, PE
and spontaneous rupture of the lens capsule may be
related to the early development of cataracts in
these individuals.
Clinically PE is noted in most reports to occur in
the first two weeks [2, 16, 17, 20, 32, 44, 45] or as
late as 'weeks' to 'months' after injury [15, 21]. In
our series of cases enucleation of eyes with PE
occurred two days to 59 years after injury and only
52% occurred in the first year. The long delay can

cause additional problems in clinical diagnosis. Re-
cently a number of patients have been reported
with a prolonged course or a delay in manifes-
tations of this disease [18, 21, 46].
Review of the literature gives the impression that
the inflammatory reaction of PE is confined to the
anterior aspect of the eye with rare or no choroidal
involvement [15, 47]. Individual case studies have
shown the choroid to be involved with a chronic,
non-granulomatous reaction [20, 40]. We found
that the choroid was involved in 76% of the cases
reviewed. The involvement of the choroid was sta-
tistically related to the severity of inflammation.
The inflammation was typically focal infiltrates of
non-granulomatous mononuclear cells, occurring
in the anterior and posterior choroid. The involve-
ment of the choroid may indicate that sensitization
to lens protein and autoimmunity to the lens may
result in an autoimmune related cross-reactivity
against other ocular tissues. Another theory is that
inflammation around the lens may be associated
with release of soluble mediators of inflammation
and a secondary reaction of the choroid.
PE may be accompanied by sympathetic oph-
thalmia [22-27]. The incidence of PE has been
reported by Blodi in 23% of 170 cases of sympa-
thetic ophthalmia [23], by Lubin et al. in 46% of
105 cases [25] and by Croxatto et al. in 14% of 100
cases [26]. There has been a dramatic decline in the
frequency of PE in cases of sympathetic ophthal-
mia since 1950. Lubin et al. note that after 1950
only 22% of the cases of sympathetic ophthalmia
studied were associated with PE and Croxatto et al.
noted a decline to 7%. They attributed this de-
crease to the improvement of the repair of pene-
trating wounds and to the use of corticosteroids as a
therapeutic agent. Of the cases of PE studied in this
series only four (2.7%) were noted to have an
associated diagnosis of sympathetic ophthalmia on
histopathologic criteria. The association between
PE and sympathetic ophthalmia can lead to confu-
sion especially in patients with a bilateral inflam-
matory reaction. Courtney [39] and deVeer [28]
have reported several cases of bilateral endoph-
thalmitis that on histopathologic review showed
classic PE, but no evidence of sympathetic ophthal-
Phacoanaphylactic endophthalmitis 277
mia. This often presents a diagnostic dilemma to
the clinician, especially if the second eye was not
subjected to trauma. There was one case in this
series with a bilateral uveitis and both eyes only
showing PE, without any histopathologic evidence
of sympathetic ophthalmia. This patient of 65 years
old had no clinical or histopathologic evidence of
trauma.
Recently Meisler et al. [48], Roussel et al. [49]
and Ormerod et al. [50] have evaluated a post-
operative endophthalmitis associated with Propio-
nibacterium aches. They note a delayed onset of
inflammation, with a chronic indolent granuloma-
tous uveitis, and difficulties in obtaining positive
cultures, all similar to PE. Because of the adjuvant
qualities of P. acnes, in promoting hypersensitivity
to lens proteins in some patients [51] and because of
the mitogenic stimulatory effects of lipopolysac-
charides, found in many bacteria, we evaluated the
presence of bacteria in several of our slides. Of the
56 slides stained for bacteria only three (5%)
showed any evidence of bacterial involvement. In
these cases the granulomatous reaction appeared
to be distinct from the major site of bacterial in-
fection, although any bacteria such as P. aches may
directly induce a granulomatous inflammation. A
so called 'pseudo-PE' may be produced as a direct
response to an intraocular lens implant. The obser-
vation of PE in proximity to lens material and
remote from the focus of infection and may be of
value in distinguishing PE from an inflammatory
response induced by an infection.
In summary, PE is a disease that in this series was
not well recognized clinically. Although, classically
occurring after trauma 20% of the cases studied
occurred spontaneously. The interval from trauma
to diagnosis reported in most studies to be 1 to 14
days was noted to be much more variable, occur-
ring 2 days to 59 years after injury. The involve-
ment of the choroid and retina indicates that the
inflammation, although centered around the lens
can involve the entire eye. The difficulty in diag-
nosis of this disease can lead to chronic inflamma-
tion with loss of vision and the loss of an eye. A high
index of suspicion for PE must be present in any
patient with a granulomatous uveitis with a recent
278 A . B . Thach et al.
or remote history of trauma, a history of microph-
thalmia or in patients who are in the age group most
likely to develop cataracts.
Acknowledgement
This study was supported in part by the Armed
Forces Institute of Pathology.
References
1. Straub M. Inflammations of the eye caused by lenticular
material dissolved in eye lymph. Amsterdam: JH DeBussy,
1919.
2. Verhoeff FH, Lemoine AN. Endophthalmitis phacoana-
phylactica. Am J Ophthalmol 1922; 5: 737-45.
3. Marak GE. Abrogation of tolerance to lens protein. In:
Sears ML (ed.) 'New directions in Ophthalmic Research'.
New Haven, Yale U. Press, pp. 47-61, 1981.
4. Marak GE, Font RL, Ward PA. Fluorescent antibody stud-
ies in experimental lens-induced granulomatous endoph-
thalmitis. Ophthal Res 1977; 9: 317-20.
5. Marak GE, Font RL, Ward FP. Arthus-type panophthal-
mitis in rats sensitized to heterologous lens protein. Oph-
thai Res 1977; 9: 162-70.
6. Marak GE, Font RL, Alepa FP. Experimental lens-in-
duced granulomatous endophthalmitis. In: Boke W. Lutz
MH (eds.) 'Ocular Immune responses'. Mod Probl Oph-
thalmol. Basel: Karger, 1976; 16: 75-9.
7. Marak GE, Font RL, Alepa FP. Experimental lens-in-
duced granulomatous endophthalmitis: Passive transfer
with serum. Ophthal Res 1976; 8: 117-20.
8. Marak GE, Font RL, Alepa FP. Immunopathogenicity of
lens crystallins in the production of experimental lens-in-
duced granulomatous endophthalmitis. Ophthal Res 1978;
10: 30-5.
9. Marak GE, Rao NA. Lens protein binding lymphocytes.
Ophthal Res 1983; 15: 6-10.
10. Marak GE, Lim LY, Rao NA. Abrogation of tolerance to
lens proteins II. Allogenic effect. Ophthal Res 1982; 14:
176-81.
11. Marak GE, Font RL, Rao NA. Abrogation of tolerance to
lens protein I. Effects of lipopolysaccharide. Ophthal Res
1979; 11: 192-8.
12. Marak GE, Font RL, Weigle WO. Pathogenesis of lens-
induced endopthalmitis. In: Silverstein AM, O'Connor GR
(eds.) 'Immunology and Immunopathology of the eye'.
New York: Masson, 1985; 135-7.
13. DeYoung LM, Spires DA, Ballaron SJ et al. Acne-like
chronic inflammatory activity of Propionibacterium aches
preparations in an animal model. Correlation with the abil-
ity to stimulate the reticuloendothelial system. J Invest
Dermatol 1985; 85: 255-8.
14. Wolter JR. Pseudophaco-anaphylactic endophthalmitis.
Graefe's Arch Clin Exp Ophthalmol 1983; 220: 160-6.
15. Zimmerman LE. Lens-induced inflammation in human
eyes. In: Maumenee AE, Silverstein AM (eds.) 'Immuno-
pathology of Uveitis'. Baltimore: Williams and Wilkins,
1964; 221-32.
16. Chan CC. Relationship between sympathetic ophthalmia,
phacoanaphylatic endophthalmitis, and Vogt-Koyanagi-
Harada disease. Ophthalmology 1988; 95: 619-24.
17. Apple DJ, Manalis N, Steinmetz RL et al. Phacoanaphylac-
tic endophthalmitis associated with extracapsular cataract
extraction and posterior chamber intraocular lens. Arch
Ophthalmol 1984; 102: 1528-32.
18. Hodes BL, Stern G. Phacoanaphylactic endophthalmitis.
Echographic diagnosis of phacoanaphylactic endophthal-
mitis. Ophthalmol Surg 1976; 7: 60-4.
19. Engel HA, Green WR, Michels RR et al. Diagnostic Vit-
rectomy. Retina 1981; I: 121-49.
20. McMahon MS, Weiss JS, Riedel KG, Albert DM. Clinical-
ly unsuspected phacoanaphylaxis after extracapsular cat-
aract extraction with intraocular lens implantation. Br J
Ophthalmol 1985; 69: 836-40.
21. Smith RE, Weiner P. Unusual presentation of phacoa-
naphylaxis following phaco-emulsification. Ophthalmol
Surg 1976; 7: 65-8,
22. deVeer JA. Endophthalmitis phacoanaphylactica and its
relation to sympathetic ophthalmia. Arch Ophthalmol
1940; 23: 23%52.
23. Blodi FC. Sympathetic uveitis as an allergic phenomenon.
Trans Am Aead Ophthal Otolaryng 1959; 63: 642-9.
24. Allen JC. Sympathetic uveitis and phacoanaphylaxis. Am J
Ophthalmol; 63: 280-3.
25. Lubin JR, Albert DM, Weinstein M. Sixty-five years of
sympathetic ophthalmia. A clinicopathologic review of 105
cases (1913-1978). Ophthalmology 1980; 87: 109-21.
26. Croxatto JO, Rao NA, McLean IW, Marak GE. Atypical
histopathologic features in sympathetic ophthalmia. Int
Ophthal 1981; 4: 129-35.
27. Easom HA, Zimmerman LE. Sympathetic ophthalmia and
bilateral phacoanaphylaxis. Arch Ophthalmol 1964; 72: 9-
15.
28. deVeer JA. Bilateral endophthalmitis phacoanaphylactica.
Pathologic study of the lesion in the eye first involved and,
in one instance, the secondarily implicated, or 'sympathiz-
ing', eye. Arch Ophthalmol 1953; 54: 607-32.
29. Hogan MJ, ZimmermanLE (eds.) 'Ophthalmic Pathology,
an Atlas and Textbook', second edition. Philadelphia: WB
Saunders. 1962: 153.
30. Spencer WH. Lens. In: Spencer WH (ed.) 'Ophthalmic
Pathology, an Atlas and Textbook', third edition. Vol 1.
Philadelphia: WB Saunders. 1985; 473-9.
31. Roberts B. In: Glass WI: Yale University Clinical Confer-
ences. Am J Ophthalmol 1957; 44: 119.

32. Riise P. Endophthalmitis phacoanaphylactica, In clinical
ophthalmology. Am J Ophthalmol 1965; 60: 911-5.
33. Apple DJ, Mamalis N, Steinmetz RL et al. Phacoanaphy-
lactic endophthalmitis following ECCE and IOL implanta-
tion. J Am Intraocul Implant Soc 1984; 10: 423-4.
34. Chandler PA. Problems in the diagnosis and treatment of
lens-induced uveitis and glaucoma. Arch Ophthalmo11958;
60: 828--41.
35. Mueller-Hermelink HK, Kraus-Mackiw E, Daus W,
Adams H. Lens as inducer and target in uveitis: comparison
of different types of naturally occurring and experimentally
induced phacogenic reactions. In: O'Connor GR, Chandler
JW (eds.) 'Advances in Immunology and Immunopathol-
ogy of the Eye'. New York: Masson, 1985; 155.
36. Wohl LG, Kline OR, Lucier AC, Galman BD. Pseudo-
phakic phacoanaphylactic endophthalmitis. Ophthalmol
Surg 1986; 17: 234--7.
37. AbrahamslW. Diagnosticandsurgicalmanagementofpha-
coanaphylactic uveitis following extracapsular cataract ex-
traction with intraocular lens implantation. J Am Intraocul
Implant Soc 1985; 11: 444.
38. Apple D J, Mamalis N, Loftfield K et al. Complications of
intraocular lenses. A historical and histopathological re-
view. Surv Ophthalmol 1984; 29: 1-54.
39. Courtney RH. Endophthalmitis with secondary glaucoma
accompanying absorption of the crystalline lens. Tr Am
Ophthalmol Soc 1942; 40: 355-69.
40. Irvine SR, Irvine AR. Lens-induced uveitis and glaucoma.
Part I. Endophthalmitis phaco-anaphylactica. Am J Oph-
thalmol 1952; 35: 177-86.
41. Chishti M, Henkind P. Spontaneous rupture of anterior
lens capsule (phacoanaphylactic endophthalmitis). Am J
Ophthalmol 1970; 69: 264-70.
42. Ford JC, Irvine AR. Persistent hyperplastic vitreous associ-
ated with anterior rupture of the lens capsule. Arch Oph-
thalmol 1961; 74: 23-30.
Phacoanaphylactic endophthalmitis 279
43. Haddad R, Font RL, Reeser F. Persistent hyperplastic
primary vitreous. A clinicopathologicstudy of 62 cases and
review of the literature. Surv Ophthalmo11978;23: 123-34.
44. Rahi AHS, Garner A. Immunopathology of the Eye. Ox-
ford, Blackwell Scientific Publications, 1976, pp. 204-20.
45. Schlaegel TF. Uveitis following cataract surgery. In: Bel-
lows JG (ed.) 'Cataract and Abnormalities of the Lens'.
New York, Grune and Stratton, 1975; 429-34.
46. Abrahms IW. Phacoanaphylaxis as a cause of granuloma-
tous uveitis following extracapsular cataract surgery. Ann
Ophthalmol 1987; 19: 211--4.
47. Muller-Hermelink HK. Recent topics in the pathology of
uveitis. In: Kraus-Mackiw E, O'Connor GR (eds.) 'Uvei-
tis: Pathophysiology and Therapy'. New York: Thieme,
1986; 152-97.
48. Meisler DM, Palestine AG, Vastine DW et al. Chronic
Propionibacterium endophthalmitis after extracapsular cat-
aract extraction and intraocular lens implantation. Am J
Ophthalmol 1986; 102: 733-9.
49. Roussel TJ, Culbertson WW, Jaffe NS. Chronic postoper-
ative endophthalmitis associated with Propionibacterium
acnes. Arch Ophthalmol 1987; 105: 1199-1201.
50. Ormerod LD, Paton BG, Haaf Jet al. Anaerobic bacterial
endophthalmitis. Ophthalmology 1987; 94: 799-808.
51. Maguire HC, Cipriano D. Immunopotentiation of cell-me-
diated hypersensitivity by Coryenbacterium parvum (Pro-
pionibacterium acnes). Int Arch Allergy Appl lmmunol
1983; 70: 34.
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