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Unilateral Eyelid Ptosis and a Red Eye
SURVEY OF OPHTHALMOLOGY VOLUME 43 • NUMBER 2 • SEPTEMBER–OCTOBER 1998
CLINICAL CHALLENGES PETER SAVINO, EDITOR
Unilateral Eyelid Ptosis and a Red Eye NIRAJ P. PATEL, MD, AND PETER J. SAVINO, MD
Neuro-Ophthalmology Service, Wills Eye Hospital, Philadelphia, Pennsylvania, USA
Comments by David A. Weinberg, MD (In keeping with the format of a clinical pathologic conference, the abstract and key words appear at the end of the article.) Case Report. A 56-year-old woman in excellent health was referred for neuro-ophthalmologic evaluation by her primary ophthalmologist because of unilateral blepharoptosis of her right upper eyelid. The patient had first noticed the onset of ptosis 2 years earlier, and she stated that it had been getting progressively worse. Despite multiple examinations, her primary ophthalmologist was unable to determine a cause. The patient also had a red eye on the ptotic side with a chronic discharge during the past year. Treatment with antibiotic drops did not relieve these symptoms. On examination the patient’s visual acuity was 20/ 40 in the right eye (pinholing to 20/25) and 20/20 in the left eye. Her pupils were equal without evidence of a relative afferent pupillary defect. Extraocular motility and confrontation fields were within normal limits. External examination showed a 3-mm ptosis of the right upper lid with an equivalent decrease in levator function in comparison with the left eye (Fig. 1). Additional testing demonstrated excellent orbicularis strength in both eyes, an absence of Cogan lid-twitch sign, and an absence of fatigue on prolonged upgaze. Anterior segment examination was significant for a marked conjunctival injection of the right eye. Intraocular pressures were 13 mm Hg in the right eye and 14 mm Hg in the left eye. The remainder of the examination, including dilated fundus examination, was within normal limits.
What are the considerations in an adult with acquired ptosis? What testing would you recommend and in what order? Would any other history be helpful?
Comments Comments by David A. Weinberg, MD, Division of Ophthalmology, Neurology, and Neurosurgery, University of Vermont School of Medicine, Burlington, Vermont, USA. This patient is a healthy 56-year-old woman with right conjunctival injection and right upper-eyelid ptosis that has progressively worsened over 1–2 years. It is worthwhile, from an academic standpoint, to review the approach to a patient who presents with blepharoptosis. Although “ptosis” may refer to the descent of any organ, for the sake of brevity in this discussion I will use the terms ptosis and blepharoptosis interchangeably, referring specifically to drooping of the upper eyelid. Ptosis has a myriad of possible causes,11 and various classification schemes have been proposed. From an anatomic viewpoint, ptosis may be myogenic, aponeurotic, neurogenic, or mechanical in etiology. Ptosis may also be classified as congenital or acquired, depending on the age at onset. Congenital ptosis is usually attributed to levator muscle maldevelopment. Depending on the pathophysio182
© 1998 by Elsevier Science Inc. All rights reserved.
0039-6257/98/$19.00 PII S0039-6257(98)00029-0
UNILATERAL PTOSIS AND RED EYE
Fig. 1. The patient in primary position (below) with right upper-lid ptosis. In upgaze after a prolonged period of time (upper) there is no increase in the ptosis. The right eye can be seen to have diffuse conjunctival injection.
logic mechanism involved, acquired ptosis may be categorized as involutional (generally caused by levator aponeurosis attenuation or dehiscence); traumatic (as a result of damage to the levator aponeurosis or muscle, or restriction of eyelid movement due to scarring); mechanical (caused by excess uppereyelid weight from edema or a mass lesion); hereditary (e.g., familial ptosis, oculopharyngeal muscular dystrophy, and congenital myasthenic syndromes); vascular (e.g., infarct, carotid-cavernous sinus fistula, or arteriovenous malformation); infectious/inflammatory/infiltrative/neoplastic (with a lesion of the anterior segment of the eye, orbit, or brain); iatrogenic (e.g., caused by topical corticosteroid eyedrops or surgery); apparent (e.g., caused by hypotropia, enophthalmos, contralateral upper-eyelid retraction, or blepharospasm); or functional. These categories overlap somewhat, and patients may have multiple mechanisms simultaneously contributing to ptosis. This list is not meant to be all-inclusive, but rather an outline for approaching the patient who presents with ptosis. Before I would recommend any testing in this patient, I would obtain more information about the pa-
183
tient’s history and physical examination. Often the history alone will direct one to the cause of the ptosis. There is no mention of any preceding eye surgery or trauma, although typical traumatic ptosis does not tend to progress. It usually either remains stable or shows spontaneous improvement. However, progressive worsening may be seen over many years, and this is likely the result of superimposed, involutional changes in the aponeurosis. Certainly, if there were a retained foreign body in the upper eyelid or orbit from a penetrating injury, then inflammation and progressive ptosis might ensue. Although the patient stated that she is “in excellent health,” patients often forget about past health problems when they are currently asymptomatic or untreated. Previous thyroidectomy for Graves disease or mastectomy for breast cancer may be relevant, even if the surgery was years ago. Although it was mentioned that “antibiotic drops did not relieve these symptoms,” there is no mention of whether or not the patient is still using any topical medications. For instance, if she were using a corticosteroid eyedrop, which is a well-established cause of ptosis, the clinical picture could be complicated by a toxic or allergic reaction to the eyedrops, producing a conjunctivitis medicamentosa. Patients will often neglect to mention the use of over-the-counter eyedrops because they were not prescribed by a physician. Family history, social history, and review of systems can offer valuable information; however, that information has not been provided in this case. Is there a family history of blepharoptosis or systemic autoimmune diseases, including thyroid disease? Familial ptosis would not explain the red eye, but there is no guarantee that these two conditions, i.e., the ptosis and the red eye, are directly related, although they probably are. It is also important to know the patient’s occupation. There may have been an injury that affected only one eye, e.g., a chemical splash or foreign-body projectile, caused by an occupational exposure. A smoking history may be relevant, as this may be associated with systemic disorders, such as Graves disease. A review of systems may disclose systemic symptoms that could be associated with this patient’s eye condition. For example, a complaint of shortness of breath might lead the physician to consider a diagnosis of sarcoidosis, particularly if uveitis or skin nodules were noted. I would be interested in knowing whether there were any signs of muscle weakness elsewhere, although normal orbicularis oculi muscle strength, absence of eyelid fatiguability on sustained upgaze, and normal extraocular motility weigh against a diagnosis of myasthenia gravis in this patient. Ptosis caused by myasthenia gravis often shows significant variability from examination to examina-
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Surv Ophthalmol 43 (2) September–October 1998
tion and even during the course of a single examination. Although a certain degree of variability and fatiguability is reported in nonmyasthenic ptosis, it is generally minimal. This patient should be (and probably was) questioned about any diplopia, and her examination should include testing for an ocular misalignment by alternate cover test. This is essential information that could help establish the underlying condition as neurologic or orbital. Because the extraocular motility was grossly full, it is rather unlikely that she had a third cranial nerve palsy, even one involving the superior division alone. Three millimeters of blepharoptosis is more than one typically sees with Horner syndrome, which is also ruled out by the absence of anisocoria. There is no mention of any obvious proptosis, but I would be interested in knowing the results of Hertel exophthalmometry and assessment of orbital resilience (i.e., resistance to retropulsion), two important indicators of orbital disease. However, the globe may be displaced vertically or horizontally with orbital disorders, so exophthalmometry does not tell the whole story. Although conjunctival injection may be associated with an orbital inflammatory process, a posterior orbital process is frequently accompanied by diplopia, extraocular motility restriction, proptosis, and/or decreased vision, which are not present in this patient. Anterior orbital inflammation, including scleritis and myositis, could be responsible, but pain and diplopia are usually more prominent in those cases than were reported in this patient.
Case Report (Continued) Dr. Weinberg’s questions and comments are appropriate and they were all addressed when the patient was examined. No pertinent positive findings were uncovered.
Comments (Continued) For the purpose of academic discussion, the previous paragraphs focused on the evaluation of acquired ptosis. However, in the evaluation of a presenting sign or symptom, it is important to pay attention to “the company it keeps” (to quote an “old” mentor of mine), i.e., other signs and symptoms. We are provided with an important associated finding, a red eye with discharge. A red eye signifies conjunctival and/or episcleral injection, which may or may not result from inflammation (ignoring the ocular discharge for the moment). There are a number of traumatic, inflammatory, infiltrative, infectious, neoplastic, vascular, and toxic/allergic conditions that can produce conjunctival injection, e.g.,
PATEL AND SAVINO
conjunctivitis, but usually without ptosis. Certainly, any condition that causes eyelid edema may result in ptosis. It is frequently helpful to know the distribution of the conjunctival hyperemia, i.e., sectoral, diffuse, superior, inferior, or circumcorneal, because this may provide an important clue to the underlying cause. Conjunctival injection that is greater superiorly might suggest superior limbic keratoconjunctivitis, a retained foreign body under the upper eyelid, giant papillary conjunctivitis, vernal conjunctivitis, or chlamydial infection with trachoma or inclusion conjunctivitis. Inferior conjunctival injection would more often be associated with conjunctivitis medicamentosa or exposure conjunctivitis caused by lagophthalmos. The photographs of this patient show what appears to be relatively mild and diffuse right conjunctival injection with right upper-eyelid ptosis and possible mild eyelid erythema. The conjunctival and episcleral vessels do not show the marked dilatation and tortuosity (caused by arterialization) typically seen with a dural arteriovenous malformation, i.e., low-flow fistula. The patient’s left upper eyelid is retracted, probably because of the right upper-eyelid ptosis, in accordance with Hering’s law. Although conjunctival hyperemia may be caused by a variety of mechanisms, including increased episcleral venous pressure, an ocular discharge implies that there is probably a component of conjunctival inflammation. Nevertheless, dacryocystitis may produce an ocular discharge. Expression of mucopurulent discharge from the punctae on palpation of the lacrimal sac will generally establish the diagnosis of dacryocystitis. Orbital or preseptal cellulitis may present as a red eye with discharge, although there were no orbital signs, e.g., proptosis or restriction of eye movement, described in this patient. While this patient’s clinical course was more protracted and subacute than is typically seen in orbital cellulitis, a chronic course such as this may be found in association with an orbital foreign body, e.g., low-grade infection of a scleral buckle. Other orbital disorders may produce an ocular discharge if there is conjunctival inflammation, anterior segment exposure caused by lagophthalmos (from proptosis or eyelid retraction), or dry eye syndrome (which may result from dacryoadenitis). There are numerous causes of chronic conjunctivitis, but certain types, such as giant papillary conjunctivitis and vernal conjunctivitis, are more often associated with ptosis. The pathophysiologic mechanism of ptosis in these cases may be contiguous inflammation of levator and/or Müller muscles when there is significant superior conjunctival inflammation. These chronic conjunctivitides are certainly in this patient’s differential diagnosis. However, vernal
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conjunctivitis is usually bilateral, and itching is typically a prominent symptom. It is important on examination to evert the upper eyelid to look for follicles, giant papillae, or a foreign body. Cultures and/or scrapings for chlamydia may be indicated, based on the appearance of the superior tarsal conjunctiva. Giant papillary conjunctivitis, which should be evident on inspection of the tarsal conjunctiva of the upper eyelid, is associated with contact lens wear, as is ptosis. The patient wore glasses when her vision was tested, but there is no mention of whether she wears contact lenses. Contact lens–associated ptosis is generally caused by repeated upper eyelid manipulation during insertion and removal of the contact lenses, likely causing a levator aponeurosis disinsertion or dehiscence. One would expect the ptosis in these cases to be bilateral if contact lenses are worn in both eyes. However, because of differences in manual dexterity in the dominant and nondominant hands, and perhaps other factors, the ptosis may be asymmetric. Contact lens–associated ptosis may also result from giant papillary conjunctivitis or a retained contact lens under the upper eyelid.13 Therefore, it is important to know whether this patient wears contact lenses. With regard to any specialized testing I might recommend, I offer the following suggestions. I would start with a thorough history and meticulous examination of the eye and ocular adnexae. With the upper eyelid everted, one should carefully inspect, using high magnification, for any retained (and possibly embedded) foreign bodies that might be contributing to the ocular surface inflammation and ptosis. Fluorescein dye may help identify a transparent or subtle foreign body, and vertical linear corneal staining is the hallmark of a foreign body beneath the upper eyelid. A thorough evaluation requires examination of the superior conjunctival fornix, using a Desmarres eyelid retractor to double evert the upper eyelid. A retained foreign body may conceal itself within the superiormost recesses of the conjunctival fornix, out of view. Even if a foreign body cannot be directly visualized, it may be worthwhile to sweep the superior conjunctival fornix with a moist, sterile cotton swab after installation of a topical anesthetic agent. Pain is usually, but not always, reported by patients with a retained foreign body under the upper eyelid. In the presence of an ocular discharge, it would be reasonable to send off a culture to isolate a potential infectious agent, and a scraping of the superior conjunctiva to identify chlamydia may be indicated (as discussed above). If proptosis, extraocular motility restriction, diplopia, or decreased vision were present or a mass were palpated, one might consider
an imaging study, either computed tomography or magnetic resonance imaging of the orbits with contrast, and bloodwork to screen for a variety of conditions. Graves ophthalmopathy usually presents with eyelid retraction, although occasionally ptosis may be seen, either with or without coincident myasthenia gravis. However, none of these suspicious findings was reported, and, therefore, I would hold off on blood work and imaging studies. I would make certain that a thorough history had been obtained and a careful examination was performed, looking for any clues to the underlying diagnosis, before deciding whether or not focused ancillary testing is indicated.
Case Report (Continued) Further questioning revealed that the patient wears soft contact lenses. She has never lost a lens, but after a contact lens fitting a few years ago, her optometrist was unable to find the right lens at the end of his examination. Lid flip was negative for a contact lens displaced superiorly in the cul-de-sac, and the patient was reassured. Her primary ophthalmologist also considered a retained contact lens, but did not find anything on his repeated examinations. Would you perform any further in-office testing?
Comments (Continued) It is now revealed that the patient wears soft contact lenses, but no mention is made of whether she wears a contact lens in one or both eyes. Above all, it is of concern that the right contact lens could not be found after a contact lens fitting “a few years ago” and that this is the patient’s symptomatic eye. A retained contact lens was not found by the patient’s optometrist or ophthalmologist. Although it is possible that the right contact lens fell onto the floor or the patient’s clothing during the fitting, strong consideration needs to be given to the possibility of a retained soft contact lens that has eluded discovery. A retained contact lens could be “hiding” deep within the superior conjunctival fornix or, theoretically, within the upper eyelid because of erosion and migration. Although a rigid contact lens may become embedded within the soft tissues of the eyelid,12 I am unaware of this having been reported with a soft contact lens. A soft lens is much more likely to adhere to the inside of the upper eyelid without penetrating the tissues. Although it seems unlikely that her primary ophthalmologist would have missed a retained contact lens on repeated examinations, I always like to take a look myself, rather than relying solely on the observations of others. This policy has been rewarding a number of times when patients have come in with a history of a normal imaging study, and repeat care-
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ful evaluation of the images has disclosed a missed lesion. Therefore, before considering an orbital imaging study (i.e., magnetic resonance imaging or computed tomography), or any other tests in this patient, I would start with the basics: inspect and palpate. If nothing were visible at the slit-lamp with the right upper eyelid everted, I would lay the patient back in the examination chair and double evert the right upper eyelid with a Desmarres eyelid retractor and inspect the far recesses of the superior conjunctival fornix with surgical loupes. Although it was stated in this patient’s case presentation that “lid flip was negative for a contact lens displaced superiorly in the cul-de-sac,” simple eversion of the upper eyelid only reveals the tarsal conjunctiva and not the superior fornix (cul-de-sac), which can be visualized only with double eversion of the eyelid. If I still did not see anything, then my last effort in the office would be to anesthetize the eye with a topical anesthetic and sweep the farthest recesses of the superior conjunctival fornix with a moist, sterile cotton swab. In addition, with the patient’s eyes gently closed, I would see whether or not I could palpate a mass through the right upper eyelid.
Case Report (Continued) and Concluding Discussion We performed double lid eversion, yielding a soft contact lens in the superior cul-de-sac of the right
PATEL AND SAVINO
eye (Fig. 2). The contact lens was easily removed with a jeweler’s forcep, and the patient was discharged on Tobradex drops four times a day. On follow-up examinations, the patient had complete resolution of her ptosis and conjunctivitis. She is currently without complaint. The phenomenon of contact lens migration into the upper-lid fornix is a rare complication of contact lens wear. Patients with “lost” contact lenses can present with a range of symptoms from no complaints to those of a swollen eyelid, an eyelid mass, a droopy eyelid, chronic discharge, or a red eye. In previously published reports, superiorly displaced hard contact lenses have been described as migrating into the upper eyelid and then embedding into the soft tissues. These patients eventually underwent surgical resection of the mass lesions with discovery of the hard contact lenses.1–10,12,13 A review of the literature has not revealed a similar experience with soft lenses. Soft contact lenses can also migrate into the superior fornix and cause localized inflammation. However, they do not appear to have a tendency to embed into the conjunctiva. In our patient, the soft contact lens induced a temporary but significant ptosis of her right upper eyelid, either caused by a localized inflammatory response or the mechanical presence of the lens. Removal of the contact lens resulted in rapid improvement of her ptosis. We are unaware of another report of a soft contact lens causing this problem.
References
Fig. 2. Soft contact lens removed from the superior cul-de-sac.
1. Benger RS, Frueh BR: An upper eyelid cyst from migration of a hard corneal contact lens. Ophthalmic Surg 17:292–294, 1986 2. Beyer-Machule CK, Shapiro A: Eyelid penetration of a hard contact lens simulating a neoplasm. Ophthalmic Surg 17: 101–102, 1986 3. Bock RH: The upper fornix trap. Br J Ophthalmol 55:784– 785, 1971 4. Brinkley JR, Zappia RJ: An eyelid tumor caused by a migrated hard contact lens. Ophthalmic Surg 11:200–202, 1980 5. Green WR: An embeded (“lost”) contact lens. Arch Ophthalmol 69:23–24, 1963 6. Jones D, Livesey S, Wilkins P: Hard contact lens migration into the upper lid. An unexpected lid lump. Br J Ophthalmol 71:368–370, 1987 7. Long JC: Retention of contact lens in upper fornix. Am J Ophthalmol 56:309, 1963 8. Michaels DD, Zugsmith GS: An unusual contact lens complication. Am J Ophthalmol 55:1057–1058, 1963 9. Nicolitz E, Flanagan JC: Orbital mass as a complication of contact lens wear. Arch Ophthalmol 96:2238–2239, 1978 10. Older JJ: Encysted corneal contact lens presenting as an eyelid mass. Ann Ophthalmol 11:1393–1394, 1979 11. Roy FH: Ocular Differential Diagnosis. Philadelphia, Lea & Febiger, 1984, ed 3, pp 32–38 12. Sebag J, Albert DM: Pseudochalazion of the upper lid due to hard contact lens embedding. Case reports and literature review. Ophthalmic Surg 13:634–636, 1982
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UNILATERAL PTOSIS AND RED EYE 13. Yassin JG, White RH, Shannon GM: Blepharoptosis as a complication of contact lens migration. Am J Ophthalmol 72: 536–537, 1971
Reprint address: Peter J Savino, MD, Wills Eye Hospital, 900 Walnut Street, Philadelphia, PA 19107, USA.
Abstract. A 56-year-old woman presented with a unilateral ptosis induced by a nonembedded soft contact lens of approximately 2 years’ duration. The unilateral ptosis most likely resulted form localized inflammation and the physical presence of the soft contact lens. The patient’s symptoms resolved completely after double lid eversion and lens removal (Surv Ophthalmol 43:182–187, 1998) © 1998 by Elsevier Science Inc. All rights reserved.) Key words. conjunctival injection • contact lens • ptosis • soft contact lens
CLINICAL CHALLENGES PETER SAVINO, EDITOR
Unilateral Eyelid Ptosis and a Red Eye NIRAJ P. PATEL, MD, AND PETER J. SAVINO, MD
Neuro-Ophthalmology Service, Wills Eye Hospital, Philadelphia, Pennsylvania, USA
Comments by David A. Weinberg, MD (In keeping with the format of a clinical pathologic conference, the abstract and key words appear at the end of the article.) Case Report. A 56-year-old woman in excellent health was referred for neuro-ophthalmologic evaluation by her primary ophthalmologist because of unilateral blepharoptosis of her right upper eyelid. The patient had first noticed the onset of ptosis 2 years earlier, and she stated that it had been getting progressively worse. Despite multiple examinations, her primary ophthalmologist was unable to determine a cause. The patient also had a red eye on the ptotic side with a chronic discharge during the past year. Treatment with antibiotic drops did not relieve these symptoms. On examination the patient’s visual acuity was 20/ 40 in the right eye (pinholing to 20/25) and 20/20 in the left eye. Her pupils were equal without evidence of a relative afferent pupillary defect. Extraocular motility and confrontation fields were within normal limits. External examination showed a 3-mm ptosis of the right upper lid with an equivalent decrease in levator function in comparison with the left eye (Fig. 1). Additional testing demonstrated excellent orbicularis strength in both eyes, an absence of Cogan lid-twitch sign, and an absence of fatigue on prolonged upgaze. Anterior segment examination was significant for a marked conjunctival injection of the right eye. Intraocular pressures were 13 mm Hg in the right eye and 14 mm Hg in the left eye. The remainder of the examination, including dilated fundus examination, was within normal limits.
What are the considerations in an adult with acquired ptosis? What testing would you recommend and in what order? Would any other history be helpful?
Comments Comments by David A. Weinberg, MD, Division of Ophthalmology, Neurology, and Neurosurgery, University of Vermont School of Medicine, Burlington, Vermont, USA. This patient is a healthy 56-year-old woman with right conjunctival injection and right upper-eyelid ptosis that has progressively worsened over 1–2 years. It is worthwhile, from an academic standpoint, to review the approach to a patient who presents with blepharoptosis. Although “ptosis” may refer to the descent of any organ, for the sake of brevity in this discussion I will use the terms ptosis and blepharoptosis interchangeably, referring specifically to drooping of the upper eyelid. Ptosis has a myriad of possible causes,11 and various classification schemes have been proposed. From an anatomic viewpoint, ptosis may be myogenic, aponeurotic, neurogenic, or mechanical in etiology. Ptosis may also be classified as congenital or acquired, depending on the age at onset. Congenital ptosis is usually attributed to levator muscle maldevelopment. Depending on the pathophysio182
© 1998 by Elsevier Science Inc. All rights reserved.
0039-6257/98/$19.00 PII S0039-6257(98)00029-0
UNILATERAL PTOSIS AND RED EYE
Fig. 1. The patient in primary position (below) with right upper-lid ptosis. In upgaze after a prolonged period of time (upper) there is no increase in the ptosis. The right eye can be seen to have diffuse conjunctival injection.
logic mechanism involved, acquired ptosis may be categorized as involutional (generally caused by levator aponeurosis attenuation or dehiscence); traumatic (as a result of damage to the levator aponeurosis or muscle, or restriction of eyelid movement due to scarring); mechanical (caused by excess uppereyelid weight from edema or a mass lesion); hereditary (e.g., familial ptosis, oculopharyngeal muscular dystrophy, and congenital myasthenic syndromes); vascular (e.g., infarct, carotid-cavernous sinus fistula, or arteriovenous malformation); infectious/inflammatory/infiltrative/neoplastic (with a lesion of the anterior segment of the eye, orbit, or brain); iatrogenic (e.g., caused by topical corticosteroid eyedrops or surgery); apparent (e.g., caused by hypotropia, enophthalmos, contralateral upper-eyelid retraction, or blepharospasm); or functional. These categories overlap somewhat, and patients may have multiple mechanisms simultaneously contributing to ptosis. This list is not meant to be all-inclusive, but rather an outline for approaching the patient who presents with ptosis. Before I would recommend any testing in this patient, I would obtain more information about the pa-
183
tient’s history and physical examination. Often the history alone will direct one to the cause of the ptosis. There is no mention of any preceding eye surgery or trauma, although typical traumatic ptosis does not tend to progress. It usually either remains stable or shows spontaneous improvement. However, progressive worsening may be seen over many years, and this is likely the result of superimposed, involutional changes in the aponeurosis. Certainly, if there were a retained foreign body in the upper eyelid or orbit from a penetrating injury, then inflammation and progressive ptosis might ensue. Although the patient stated that she is “in excellent health,” patients often forget about past health problems when they are currently asymptomatic or untreated. Previous thyroidectomy for Graves disease or mastectomy for breast cancer may be relevant, even if the surgery was years ago. Although it was mentioned that “antibiotic drops did not relieve these symptoms,” there is no mention of whether or not the patient is still using any topical medications. For instance, if she were using a corticosteroid eyedrop, which is a well-established cause of ptosis, the clinical picture could be complicated by a toxic or allergic reaction to the eyedrops, producing a conjunctivitis medicamentosa. Patients will often neglect to mention the use of over-the-counter eyedrops because they were not prescribed by a physician. Family history, social history, and review of systems can offer valuable information; however, that information has not been provided in this case. Is there a family history of blepharoptosis or systemic autoimmune diseases, including thyroid disease? Familial ptosis would not explain the red eye, but there is no guarantee that these two conditions, i.e., the ptosis and the red eye, are directly related, although they probably are. It is also important to know the patient’s occupation. There may have been an injury that affected only one eye, e.g., a chemical splash or foreign-body projectile, caused by an occupational exposure. A smoking history may be relevant, as this may be associated with systemic disorders, such as Graves disease. A review of systems may disclose systemic symptoms that could be associated with this patient’s eye condition. For example, a complaint of shortness of breath might lead the physician to consider a diagnosis of sarcoidosis, particularly if uveitis or skin nodules were noted. I would be interested in knowing whether there were any signs of muscle weakness elsewhere, although normal orbicularis oculi muscle strength, absence of eyelid fatiguability on sustained upgaze, and normal extraocular motility weigh against a diagnosis of myasthenia gravis in this patient. Ptosis caused by myasthenia gravis often shows significant variability from examination to examina-
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Surv Ophthalmol 43 (2) September–October 1998
tion and even during the course of a single examination. Although a certain degree of variability and fatiguability is reported in nonmyasthenic ptosis, it is generally minimal. This patient should be (and probably was) questioned about any diplopia, and her examination should include testing for an ocular misalignment by alternate cover test. This is essential information that could help establish the underlying condition as neurologic or orbital. Because the extraocular motility was grossly full, it is rather unlikely that she had a third cranial nerve palsy, even one involving the superior division alone. Three millimeters of blepharoptosis is more than one typically sees with Horner syndrome, which is also ruled out by the absence of anisocoria. There is no mention of any obvious proptosis, but I would be interested in knowing the results of Hertel exophthalmometry and assessment of orbital resilience (i.e., resistance to retropulsion), two important indicators of orbital disease. However, the globe may be displaced vertically or horizontally with orbital disorders, so exophthalmometry does not tell the whole story. Although conjunctival injection may be associated with an orbital inflammatory process, a posterior orbital process is frequently accompanied by diplopia, extraocular motility restriction, proptosis, and/or decreased vision, which are not present in this patient. Anterior orbital inflammation, including scleritis and myositis, could be responsible, but pain and diplopia are usually more prominent in those cases than were reported in this patient.
Case Report (Continued) Dr. Weinberg’s questions and comments are appropriate and they were all addressed when the patient was examined. No pertinent positive findings were uncovered.
Comments (Continued) For the purpose of academic discussion, the previous paragraphs focused on the evaluation of acquired ptosis. However, in the evaluation of a presenting sign or symptom, it is important to pay attention to “the company it keeps” (to quote an “old” mentor of mine), i.e., other signs and symptoms. We are provided with an important associated finding, a red eye with discharge. A red eye signifies conjunctival and/or episcleral injection, which may or may not result from inflammation (ignoring the ocular discharge for the moment). There are a number of traumatic, inflammatory, infiltrative, infectious, neoplastic, vascular, and toxic/allergic conditions that can produce conjunctival injection, e.g.,
PATEL AND SAVINO
conjunctivitis, but usually without ptosis. Certainly, any condition that causes eyelid edema may result in ptosis. It is frequently helpful to know the distribution of the conjunctival hyperemia, i.e., sectoral, diffuse, superior, inferior, or circumcorneal, because this may provide an important clue to the underlying cause. Conjunctival injection that is greater superiorly might suggest superior limbic keratoconjunctivitis, a retained foreign body under the upper eyelid, giant papillary conjunctivitis, vernal conjunctivitis, or chlamydial infection with trachoma or inclusion conjunctivitis. Inferior conjunctival injection would more often be associated with conjunctivitis medicamentosa or exposure conjunctivitis caused by lagophthalmos. The photographs of this patient show what appears to be relatively mild and diffuse right conjunctival injection with right upper-eyelid ptosis and possible mild eyelid erythema. The conjunctival and episcleral vessels do not show the marked dilatation and tortuosity (caused by arterialization) typically seen with a dural arteriovenous malformation, i.e., low-flow fistula. The patient’s left upper eyelid is retracted, probably because of the right upper-eyelid ptosis, in accordance with Hering’s law. Although conjunctival hyperemia may be caused by a variety of mechanisms, including increased episcleral venous pressure, an ocular discharge implies that there is probably a component of conjunctival inflammation. Nevertheless, dacryocystitis may produce an ocular discharge. Expression of mucopurulent discharge from the punctae on palpation of the lacrimal sac will generally establish the diagnosis of dacryocystitis. Orbital or preseptal cellulitis may present as a red eye with discharge, although there were no orbital signs, e.g., proptosis or restriction of eye movement, described in this patient. While this patient’s clinical course was more protracted and subacute than is typically seen in orbital cellulitis, a chronic course such as this may be found in association with an orbital foreign body, e.g., low-grade infection of a scleral buckle. Other orbital disorders may produce an ocular discharge if there is conjunctival inflammation, anterior segment exposure caused by lagophthalmos (from proptosis or eyelid retraction), or dry eye syndrome (which may result from dacryoadenitis). There are numerous causes of chronic conjunctivitis, but certain types, such as giant papillary conjunctivitis and vernal conjunctivitis, are more often associated with ptosis. The pathophysiologic mechanism of ptosis in these cases may be contiguous inflammation of levator and/or Müller muscles when there is significant superior conjunctival inflammation. These chronic conjunctivitides are certainly in this patient’s differential diagnosis. However, vernal
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conjunctivitis is usually bilateral, and itching is typically a prominent symptom. It is important on examination to evert the upper eyelid to look for follicles, giant papillae, or a foreign body. Cultures and/or scrapings for chlamydia may be indicated, based on the appearance of the superior tarsal conjunctiva. Giant papillary conjunctivitis, which should be evident on inspection of the tarsal conjunctiva of the upper eyelid, is associated with contact lens wear, as is ptosis. The patient wore glasses when her vision was tested, but there is no mention of whether she wears contact lenses. Contact lens–associated ptosis is generally caused by repeated upper eyelid manipulation during insertion and removal of the contact lenses, likely causing a levator aponeurosis disinsertion or dehiscence. One would expect the ptosis in these cases to be bilateral if contact lenses are worn in both eyes. However, because of differences in manual dexterity in the dominant and nondominant hands, and perhaps other factors, the ptosis may be asymmetric. Contact lens–associated ptosis may also result from giant papillary conjunctivitis or a retained contact lens under the upper eyelid.13 Therefore, it is important to know whether this patient wears contact lenses. With regard to any specialized testing I might recommend, I offer the following suggestions. I would start with a thorough history and meticulous examination of the eye and ocular adnexae. With the upper eyelid everted, one should carefully inspect, using high magnification, for any retained (and possibly embedded) foreign bodies that might be contributing to the ocular surface inflammation and ptosis. Fluorescein dye may help identify a transparent or subtle foreign body, and vertical linear corneal staining is the hallmark of a foreign body beneath the upper eyelid. A thorough evaluation requires examination of the superior conjunctival fornix, using a Desmarres eyelid retractor to double evert the upper eyelid. A retained foreign body may conceal itself within the superiormost recesses of the conjunctival fornix, out of view. Even if a foreign body cannot be directly visualized, it may be worthwhile to sweep the superior conjunctival fornix with a moist, sterile cotton swab after installation of a topical anesthetic agent. Pain is usually, but not always, reported by patients with a retained foreign body under the upper eyelid. In the presence of an ocular discharge, it would be reasonable to send off a culture to isolate a potential infectious agent, and a scraping of the superior conjunctiva to identify chlamydia may be indicated (as discussed above). If proptosis, extraocular motility restriction, diplopia, or decreased vision were present or a mass were palpated, one might consider
an imaging study, either computed tomography or magnetic resonance imaging of the orbits with contrast, and bloodwork to screen for a variety of conditions. Graves ophthalmopathy usually presents with eyelid retraction, although occasionally ptosis may be seen, either with or without coincident myasthenia gravis. However, none of these suspicious findings was reported, and, therefore, I would hold off on blood work and imaging studies. I would make certain that a thorough history had been obtained and a careful examination was performed, looking for any clues to the underlying diagnosis, before deciding whether or not focused ancillary testing is indicated.
Case Report (Continued) Further questioning revealed that the patient wears soft contact lenses. She has never lost a lens, but after a contact lens fitting a few years ago, her optometrist was unable to find the right lens at the end of his examination. Lid flip was negative for a contact lens displaced superiorly in the cul-de-sac, and the patient was reassured. Her primary ophthalmologist also considered a retained contact lens, but did not find anything on his repeated examinations. Would you perform any further in-office testing?
Comments (Continued) It is now revealed that the patient wears soft contact lenses, but no mention is made of whether she wears a contact lens in one or both eyes. Above all, it is of concern that the right contact lens could not be found after a contact lens fitting “a few years ago” and that this is the patient’s symptomatic eye. A retained contact lens was not found by the patient’s optometrist or ophthalmologist. Although it is possible that the right contact lens fell onto the floor or the patient’s clothing during the fitting, strong consideration needs to be given to the possibility of a retained soft contact lens that has eluded discovery. A retained contact lens could be “hiding” deep within the superior conjunctival fornix or, theoretically, within the upper eyelid because of erosion and migration. Although a rigid contact lens may become embedded within the soft tissues of the eyelid,12 I am unaware of this having been reported with a soft contact lens. A soft lens is much more likely to adhere to the inside of the upper eyelid without penetrating the tissues. Although it seems unlikely that her primary ophthalmologist would have missed a retained contact lens on repeated examinations, I always like to take a look myself, rather than relying solely on the observations of others. This policy has been rewarding a number of times when patients have come in with a history of a normal imaging study, and repeat care-
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ful evaluation of the images has disclosed a missed lesion. Therefore, before considering an orbital imaging study (i.e., magnetic resonance imaging or computed tomography), or any other tests in this patient, I would start with the basics: inspect and palpate. If nothing were visible at the slit-lamp with the right upper eyelid everted, I would lay the patient back in the examination chair and double evert the right upper eyelid with a Desmarres eyelid retractor and inspect the far recesses of the superior conjunctival fornix with surgical loupes. Although it was stated in this patient’s case presentation that “lid flip was negative for a contact lens displaced superiorly in the cul-de-sac,” simple eversion of the upper eyelid only reveals the tarsal conjunctiva and not the superior fornix (cul-de-sac), which can be visualized only with double eversion of the eyelid. If I still did not see anything, then my last effort in the office would be to anesthetize the eye with a topical anesthetic and sweep the farthest recesses of the superior conjunctival fornix with a moist, sterile cotton swab. In addition, with the patient’s eyes gently closed, I would see whether or not I could palpate a mass through the right upper eyelid.
Case Report (Continued) and Concluding Discussion We performed double lid eversion, yielding a soft contact lens in the superior cul-de-sac of the right
PATEL AND SAVINO
eye (Fig. 2). The contact lens was easily removed with a jeweler’s forcep, and the patient was discharged on Tobradex drops four times a day. On follow-up examinations, the patient had complete resolution of her ptosis and conjunctivitis. She is currently without complaint. The phenomenon of contact lens migration into the upper-lid fornix is a rare complication of contact lens wear. Patients with “lost” contact lenses can present with a range of symptoms from no complaints to those of a swollen eyelid, an eyelid mass, a droopy eyelid, chronic discharge, or a red eye. In previously published reports, superiorly displaced hard contact lenses have been described as migrating into the upper eyelid and then embedding into the soft tissues. These patients eventually underwent surgical resection of the mass lesions with discovery of the hard contact lenses.1–10,12,13 A review of the literature has not revealed a similar experience with soft lenses. Soft contact lenses can also migrate into the superior fornix and cause localized inflammation. However, they do not appear to have a tendency to embed into the conjunctiva. In our patient, the soft contact lens induced a temporary but significant ptosis of her right upper eyelid, either caused by a localized inflammatory response or the mechanical presence of the lens. Removal of the contact lens resulted in rapid improvement of her ptosis. We are unaware of another report of a soft contact lens causing this problem.
References
Fig. 2. Soft contact lens removed from the superior cul-de-sac.
1. Benger RS, Frueh BR: An upper eyelid cyst from migration of a hard corneal contact lens. Ophthalmic Surg 17:292–294, 1986 2. Beyer-Machule CK, Shapiro A: Eyelid penetration of a hard contact lens simulating a neoplasm. Ophthalmic Surg 17: 101–102, 1986 3. Bock RH: The upper fornix trap. Br J Ophthalmol 55:784– 785, 1971 4. Brinkley JR, Zappia RJ: An eyelid tumor caused by a migrated hard contact lens. Ophthalmic Surg 11:200–202, 1980 5. Green WR: An embeded (“lost”) contact lens. Arch Ophthalmol 69:23–24, 1963 6. Jones D, Livesey S, Wilkins P: Hard contact lens migration into the upper lid. An unexpected lid lump. Br J Ophthalmol 71:368–370, 1987 7. Long JC: Retention of contact lens in upper fornix. Am J Ophthalmol 56:309, 1963 8. Michaels DD, Zugsmith GS: An unusual contact lens complication. Am J Ophthalmol 55:1057–1058, 1963 9. Nicolitz E, Flanagan JC: Orbital mass as a complication of contact lens wear. Arch Ophthalmol 96:2238–2239, 1978 10. Older JJ: Encysted corneal contact lens presenting as an eyelid mass. Ann Ophthalmol 11:1393–1394, 1979 11. Roy FH: Ocular Differential Diagnosis. Philadelphia, Lea & Febiger, 1984, ed 3, pp 32–38 12. Sebag J, Albert DM: Pseudochalazion of the upper lid due to hard contact lens embedding. Case reports and literature review. Ophthalmic Surg 13:634–636, 1982
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Reprint address: Peter J Savino, MD, Wills Eye Hospital, 900 Walnut Street, Philadelphia, PA 19107, USA.
Abstract. A 56-year-old woman presented with a unilateral ptosis induced by a nonembedded soft contact lens of approximately 2 years’ duration. The unilateral ptosis most likely resulted form localized inflammation and the physical presence of the soft contact lens. The patient’s symptoms resolved completely after double lid eversion and lens removal (Surv Ophthalmol 43:182–187, 1998) © 1998 by Elsevier Science Inc. All rights reserved.) Key words. conjunctival injection • contact lens • ptosis • soft contact lens