Blepharoptosis Induced by Prolong ed Hard Contact Lens Wear Willem A van den Bosch, MD, Hans G. Lemij, MD, PhD
Purpose: The authors attempt to establish a relation between hard contact lens wear and upper eyelid ptosis. Methods: This study consists of two parts. In the first part, the authors compare the unilateral or bilateral ptosis that developed during hard contact lens wear in 17 patients with the involutional ptosis that developed in another group of 73 patients. In the second part, the authors compare both upper and lower eyelid position in 46 patients who had been wearing hard contact lenses for at least 10 years with the position of 50 matched controls who had never worn contact lenses. Results: The ptosis that had developed in the 17 patients who wore hard contact lenses was clinically similar to that caused by involutional levator disinsertion. The second part of the study shows that the prolonged wearers of hard contact lenses had upper eyelids that were lower by approximately 0.5 mm when compared with control subjects. This difference is statistically significant. According to standard criteria, there were at least 10 ptotic eyelids in the contact lens group versus 1 in the control group. Conclusion: The study findings suggest that prolonged hard contact lens wear may induce a lower position of the upper eyelid and eventually lead to ptosis through levator disinsertion. Ophthalmology 1992;99: 1759-1765
Disinsertion or thinning of the levator aponeurosis causes ptosis of the upper eyelid. 1-4 The commonest causes of levator disinsertion are trauma and involutional changes. The most frequent traumatic cause of disinsertion of the levator aponeurosis is intraocular surgery. 3 Traction on the eyelid during surgery, postoperative edema, and at teinpts made by the patient to open a patched eye after surgery all have been implicated as factors causing trau matic levator disinsertion. 2•3 In involutional ptosis, the process of aging causes thinning or disinsertion of the levator aponeurosis. Other factors that have been men tioned as possibly related to involutional ptosis through thinning or disinsertion of the levator aponeurosis are Originally received: March 13, 1992. Revision accepted: July 14, 1992. From the Eye Hospital Rotterdam, Rotterdam, The Netherlands. Reprint requests to Willem A. van den Bosch, MD, Eye Hospital Rot terdam, Schiedamsevest 180, 30 II BH Rotterdam, The Netherlands.
2 ocular inflammation and topically applied steroids. For brevity, we shall henceforth refer to any ptosis caused by thinning or disinsertion of the levator aponeurosis as apo neurogenic ptosis. The clinical picture of aponeurogenic ptosis of any cause is typical: the function of the levator muscle is good ( 12 mm or greater), and the ptotic eyelid shows a high skin crease. 2 .4,s The high skin crease develops because the posterior fibers of the levator aponeurosis on the tarsal plate disinsert or lengthen, while the anterior insertion of the levator aponeurosis into the orbicularis muscle and skin remains intact. 6 Occasionally, thinning of the eyelid can be observed. 2 The current treatment of choice of le vator disinsertion is the surgical reinsertion of the levator aponeurosis, if necessary combined with the reconstruc tion of the skin crease.I.3·4 •7•8 Thinning, disinsertion, or defects of the levator aponeurosis often can be recognized during surgical correction. 1 If it remains unclear whether a ptosis is aponeurogenic, other causes, such as inflammatory disorders of the con
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junctiva, muscular dystrophies, and neurologic disease, must be ruled out. 3 •6 •9 • 10 In addition, blepharospasm, pos sibly caused by photophobia secondary to conjunctivitis, must be excluded. 9·' 0 Ptosis caused by both vernal and giant papillary conjunctivitis also has been described. 9· 10 Importantly, hard contact lens wear as a possible cause of ptosis without tarsal conjunctival changes has, to our knowledge, only been reported twice. Its pathogenesis, however, remains a mystery. In one report, ptosis devel oped within a few weeks when habitual, daily-wear contact lens wearers exchanged their hard or soft lenses for ex tended-wear hard lenses. In these cases, the ptosis disap peared within a few weeks after switching back to the previous, daily-wear lens type. 11 This reversibility pre cludes that the ptosis in these cases was aponeurogenic. In another series, five patients with eight ptotic eyelids were described. 12 These patients had both the clinical and the intraoperative signs of ptosis through levator disin sertion. In the first part of the current report, we confirm and extend these reports by describing 17 patients who de veloped a ptosis while wearing hard contact lenses for at least 3 years. To further investigate the relation between prolonged wearing of hard contact lenses and ptosis, we examined a group of habitual wearers of such lenses and compared the position of their eyelids with that of a matched control group. None of the contact lens wearers complained of any ptosis. We found that the position of the upper eyelid was indeed lower by approximately 0.5 mm in the contact lens wearers group compared with the controls. Some of the data ofour asymptomatic hard con tact lens wearers even satisfied the set criteria of ptosis. Our findings strongly support the notion that hard contact lenses play a role in the development of ptosis through levator disinsertion.
Patients with Contact Lens Related Ptosis Patients and Methods Between January 1990 and November I99I, I7 long-term wearers of hard contact lenses sought treatment for bleph aroptosis that had developed in one or both upper eyelids. All patients were carefully examined to assess the cause of their ptosis. Levator function was 12 mm or more in all cases. If the ptosis was severe, the skin crease was high. We did not observe any signs of congenital ptosis, such as lid-lag on downgaze. No abnormalities of the tarsal plate or upper fornix, which could have caused the ptosis, were seen. No signs indicative of a muscular or neuro muscular disorder that might cause the ptosis, such as lid twitch or worsening of the ptosis after sustained upgaze, were found. None of these patients had photophobia or excessive blinking, which might possibly be associated with blepharospasm due to conjunctivitis. 9•10 On slit-lamp examination, all corneas were clear. In conclusion, we found no abnormalities other than ptosis that, on clinical examination, showed the picture of aponeurogenic ptosis.
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All but 2 patients stated that the ptosis had developed gradually during the last I or 2 years, and most patients could illustrate this with photographs. In the other 2 pa tients, the ptosis had existed for 6 and 16 years, respec tively, and had become gradually worse. The patients were between 18 and 56 years ofage (mean age, 38.5 years). There were 14 females and 3 males. Fif teen of the patients wore hard contact lenses bilaterally; one patient wore only one hard contact lens and had a ptosis on that side, whereas another patient wore a hard lens on one side, and a soft lens on the other. She had a ptosis on the side in which the hard lens was worn. In total, 32 hard contact lenses were worn in our group. The wearing time of the lenses varied from 3 to 27 years (mean wearing time, 15.2 years). Two patients used a suction cup to remove the hard contact lenses from their eyes. All other patients removed their lenses by blinking force fully while pulling their eyelids laterally. All patients were photographed with a camera mounted with a 135-mm macro lens. The patients were asked to look at the lens center when the pictures were taken. These pictures were later used to measure the upper eyelid height. The height ofthe upper eyelid was expressed in millimeters as the upper margin reflex distance, which was, by defi nition, the distance between the center of the pupil and the lower margin of the upper eyelid. The horizontal cor neal diameter served as a calibration reference for the measurements; it was assumed to have a magnitude of 11.8 mm, since this was the average value found in the second part of this study (see below). The photographs of 3 patients are shown in Figures 1 to 3. Figure 1A shows the typical clinical picture of a bilateral ptosis through levator disinsertion of a 47-year old patient who had worn hard contact lenses for 24 years. Figure IB shows the same patient 1 week after successful surgical anterior levator reinsertion. Figure 2 shows a 23 year-old patient who developed a right-sided ptosis after 6 years of bilateral hard contact lens wear. Figure 3 shows a 23-year-old patient who had been wearing a hard contact lens on the right side and a soft contact lens on the left side for 7 years; note that she had developed a ptosis on the side of the hard contact lens.
Results The upper margin reflex distances of all 34 eyelids in our I7 patients are depicted in Figure 4. For a clear assessment of these data, we have set a criterion for ptosis at an upper margin reflex distance of less than 2.8 mm. This value equals the mean upper mar gin reflex distance minus twice its standard deviation as found in control subjects in the second part of our study, to be described. For clarity, we have added a line in Figure 4, which represents the criterion of 2.8 mm. According to this criterion, there were 24 ptotic eyelids in our study. If we include 1 more patient who had an upper margin reflex distance of more than 3 mm, but who showed an asymmetry of 2 mm between the two upper eyelids, there were 25 cases.
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear
Figure 1. A, a typical, 47-year-old patient who had been wearing hard contact lenses for 24 years. Her bilateral ptosis with high skin crease is prominent. B, 1 week after anterior levator reinsertion.
To date, surgical correction has been performed in I 0 patients. This was done by reinserting the levator apo neurosis on the anterior surface of the tarsal plate under local anesthesia and reconstructing the skin crease. 8 Dur ing surgery, we observed disinsertion of the levator apo neurosis in both upper eyelids of one patient and a very thin levator aponeurosis in both upper eyelids offive other patients. The operative procedure was successful in all I0 patients. To distinguish this group from another group of pa tients with involutional ptosis, we compared the age dis tribution of the first group with that of a group of 73 patients with involutional ptosis who were seen in the eyelid clinic during the same period. In this group, no reasons other than levator disinsertion secondary to in volutional changes were present (i.e., no previous intra ocular or eyelid surgery, no contact lens wear, etc.). They were between 48 and 88 years ofage (mean age, 69 years). Figure 5 shows the age distribution of the two groups. There is only a slight overlap in age between the two groups, which strongly suggests that disinsertion of the levator aponeurosis associated with hard contact lens wear is a distinct category.
Figure 2. A 23-year-old patient who had developed a right-sided ptosis during 6 years of bilateral hard contact lens wear.
Eyelid Position After Prolonged Hard Contact Lens Wear Compared with a Matched Control Group Subjects and Methods In the first part of this study, we demonstrated that apo neurogenic blepharoptosis may be associated with pro longed use of hard contact lenses. It is as yet unclear whether a lowering of the upper eyelid occurs in all hard contact lens wearers or whether this will happen only in susceptible individuals. Therefore, we photographed and investigated 50 consecutive patients at our contact lens department who had been wearing hard contact lenses in both eyes for at least 10 years (average period, 16.3 years). These patients were matched for age and sex with 50 con trols. In the contact lens group, the mean age was 35.4 years with a standard deviation (SD) of 7.5 years. The mean age of the control group was 35.6 years with an SD of7.4 years. Everyone in either group had a bilateral visual acuity of 20/20 or better with optical correction (contact
Figure 3. A 23-year-old patient who had been wearing a hard contact lens on the right and a soft contact lens on the left side for 7 years. She had developed a ptosis on the side of the hard contact lens.
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lenses or spectacles), if required. In both groups, exclusion criteria were any corneal pathology, any ophthalmologic operation, family history of ptosis, any previous ocular inflammatory disease, use of eyedrops, and diseases that might influence eyelid position (allergies, hay fever, facial palsy, Graves disease, neurologic and muscle diseases). After obtaining informed consent and a detailed his tory, the eyelids were photographed. To photograph the subjects, we used a chin rest and instrument table previ ously used for a keratometer. On the instrument table, a camera with a 50-mm macro lens and a flash unit were fitted instead of the keratometer. The focal distance of the lens was fixed at 30 em. Eight photographic slides were taken of each contact lens wearer: two of each eye while wearing the contact lens and two ofeach eye shortly after removing the contact lens. In the control group, two photographic slides of each eye were taken. To obtain comparable measurements, great care was taken to align the optical axis of the camera with the corneal center, and each subject was requested to look at the center of the camera lens. After photographing the eyes, we everted the upper eyelids. Subjects with abnormalities of the tarsal plate (follicles, papillary conjunctivitis, scars) were excluded from our study. The slides were projected onto the screen of an Agfa Copex LP3 projector (Agfa Gevaert, Leverkusen, Ger many), which produced a magnification of six times life size. The corneal center was determined by centering a set of concentric circles on the pupil. On each slide, the horizontal corneal diameter and the upper margin reflex distance were measured. In addition, the distance between pupil center and lower eyelid margin was measured. These measurements all were performed by the same technician, who was not aware of the working hypothesis of the study. The measurements on the individual slides were repro 7 6
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ducible with an accuracy better than 0.15 mm. Two slides were available for each measurement; their averaged re sults served as final data for each eyelid. From the contact lens group, the results from four pa tients could not be used for several reasons. Thus, mea surements of only 46 patients (92 eyes) were used for this study. In the control group, results from all 50 subjects were used.
Results The upper eyelid margin was, on average, 0.5-mm lower in hard contact lens wearers than in subjects in the control group (P < 0.0015, Wilcoxon rank sum test). Figure 6A shows the distribution ofthe upper margin reflex distance both in the contact lens wearers and in the control subjects. It is evident from Figure 6A that the distribution of the upper margin reflex distance in the contact lens wear ers is shifted toward a lower (i.e., more ptotic) position compared with the control subjects. In the control group, the mean upper margin reflex distance was 4.2 mm (SD = 0.7 mm), while in the contact lens wearers group it averaged 3.7 mm (SD = 1.0 mm). Shortly after the hard contact lenses were removed, the position of the upper eyelids did not change significantly (Figs 6A and 6B). Be cause the upper margin reflex distance distribution in the control group assumes a pseudo-Gaussian curve, we de termined a standard criterion for ptosis by subtracting twice the standard deviation from the mean upper margin reflex distance. This standard criterion equaled 2.8 mm (4.2- [2 X 0.7]). For clarity, we have drawn a line at this criterion of 2.8 mm in Figures 6A and 6B. Adopting this criterion, we found 10 ptotic eyelids in the hard contact lens group while wearing the lens, and 1 more shortly after the lenses were removed. In contrast, there was only 1 ptotic eyelid in the control group. Note that none of our 96 subjects complained of any ptosis. Figures 7A and 7B show the lower margin reflex dis tances (i.e., the distance between the pupil center and the
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear
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lower eyelid margin) ofthe hard contact lens wearers both with their lenses in and shortly after lens removal, re spectively. For comparison, the data of the control group are also presented in the same figures. No significant dif ference in lower eyelid position was found between contact lens wearers and the control group. Also, no significant difference in lower eyelid position was found in the contact lens group between measurements during hard contact lens wear and measurements after lens removal. The av erage lower margin reflex distance was 5.8 mm before lens removal (SD = 0.8 mm), and also 5.8 mm (SD = 0.7 mm) after lens removal.
Discussion To date, detailed reports on ptosis associated with the long-term wearing of hard contact lenses have been fairly scarce. We have tried to fill the gap somewhat by reporting on 17 patients with such a ptosis. This hard contact lens related ptosis resembled clinically the picture of a ptosis due to disinsertion or thinning of the levator aponeurosis.
Moreover, such thinning or disinsertion was actually ob served in several of our operated patients. We ruled out the possibility that our results were confounded by other, well-known, causes of levator thinning or disinsertion, such as surgical trauma or involutional, degenerative changes. Our study of eyelid position in normal, habitual, long term hard-contact lens wearers shows clearly that the up per eyelid may sag approximately 0.5 mm compared with matched controls. This has, to our knowledge, not been reported previously. Importantly, even a considerable number of our asymptomatic, long-term wearers of hard contact lenses had actually developed an outright ptosis. Perhaps the sagging of the upper eyelid develops so slowly in habitual wearers of hard contact lenses that it passes unnoticed for a long period of time. These results bring up the question how the wearing of hard contact lenses may bring about such changes to the levator aponeurosis. It is generally accepted that ex cessive traction on the upper eyelid, such as occurs with ocular surgery or with eyelid edema, may result in a dis insertion of the levator aponeurosis. 2 Most of our contact
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Figure 7. As Figure 6, for lower eyelid position.
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lens wearers took out their lenses by pulling the eyelid laterally. This traction is essentially different from the or thogonally directed traction associated with ocular surgery and edema. Therefore, one would expect this to cause a disinsertion, if any, of the lateral canthal ligament or me dial canthal tendon, but not of the levator aponeurosis proper. However, this practice of lens removal may still play a significant role in thinning or disinserting the levator aponeurosis: while the eyelid is pulled laterally the patient squeezes the lens out by blinking. Possibly, both the or bicularis and the levator muscle then contract simulta neously, because the eye has to be wide open, while a powerful blink is made. This antagonistic action of the orbicularis and levator muscle might exert increased trac tion on the levator aponeurosis, finally leading to its dis insertion. The same procedure of! ens removal also might damage the levator aponeurosis through another mechanism. If the attempt to remove a lens fails, the lens presumably will rub forcefully over the palpebral conjunctiva, thereby stretching it and the underlying structures, such as the levator aponeurosis. We therefore speculate that failed attempts to remove a hard contact lens by sideward pulling of the eyelids and blinking may yield disinsertion or thin ning of the levator aponeurosis. These mechanisms may have played a role in the series described by Epstein and Putterman. 12 Of the five patients who developed a ptosis during hard contact lens wear, two patients developed the ptosis directly after they were fitted with hard lenses. The ptosis in these cases was not reversible. Obviously, the use of a suction cup to remove the lenses would not have this effect. Interestingly, there were two patients in our study who used a suction cup for lens removal who had nonetheless developed a ptosis. Therefore, at least one other mecha nism should be held responsible for the sagging of the upper eyelid in some hard contact lens wearers. One might argue that every blink made during the reg ular wearing of hard contact lenses rubs the lens against the eyelid structures. This repeated rubbing may finally cause levator disinsertion much in the same way as de scribed above. In this mechanism, the way in which the contact lenses are fitted, as well as the position of the contact lens on the eyeball, may play a role. We did not investigate these aspects in our patients, although they might, in future, be of great potential interest. Also, irritation ofthe eyelid by the lens may cause eyelid edema and ptosis due to the force of gravity. This ptosis would be reversible in a beginning stage, since discontin ued wearing of the lens would take away the irritation, allowing the eyelid to slim to its original proportions. It may be that this mechanism played a role in the cases described by Fonn and Holden, 11 who fitted 11 long-term wearers of hard or soft contact lenses with an extended wear hard contact lenses in one eye. Approximately half of their group developed a ptosis within 4 weeks, which again disappeared within 2 to 4 weeks after cessation of wearing the extended-wear lens. 11 Irritation might not only produce swelling and subse quent ptosis, it also might induce reflex blepharospasm.
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This could, along similar lines, account for the ptosis ob served by Fonn and Holden .'' In addition, it could be responsible for the ptosis in our patients, as well as for the lower position of the upper eyelid observed in our long-term wearers of hard contact lenses. Prolonged spasm of the orbicularis could strain the levator muscle or could cause, in turn, a higher tonus of the levator muscle. Blepharospasm would not only cause a lower position of the upper eyelid, but also a higher position of the lower eyelid. Interestingly, we did not find a difference in lower eyelid position between long-term lens wearers and con trols. Also, there was no change in upper eyelid position directly after lens removal. Therefore, blepharospasm ap pears to be a less likely cause of sagged upper eyelids in wearers of hard contact lenses. In summary, at least five different mechanisms can be tentatively put forward through which disinsertion and thinning of the levator aponeurosis in hard contact lens related ptosis may possibly come about. These are: (1) simultaneous, although antagonistic, action of the orbi cularis and levator muscle while squeezing the eyelids to remove the lens; (2) forceful rubbing of the lens and sub sequent stretching of upper eyelid structures during failed attempts of lens removal; (3) repeated and similar, al though less forceful, rubbing of the lens during blinking; (4) irritation, leading to edema; and (5) irritation leading to blepharospasm. It is, as yet, not clear to what extent these presumed mechanisms add, if anything, to the ptosis. Our results bring up another interesting question. Does the hard contact lens-related ptosis develop only in sus ceptible individuals, or does every wearer of such lenses eventually run an equal risk? We have reported, for the first time, that habitual wearers of hard contact lenses have upper eyelids that sag, on average, 0.5 mm compared with matched controls. We do not know, however, to what extent this sagging is reversible or by what mechanism it is caused. If it were reversible, this would surely be of great interest to those with marked sagging. We have in sufficient evidence to attribute this sagging to a thinning or disinsertion of the levator aponeurosis. Such a possi bility, however, by the same token, cannot be excluded. Prolonged wearing of hard contact lenses will nonetheless lead, in some individuals, to a ptosis due to damage to the levator aponeurosis. Importantly, we believe that we come across such ptosis ever more frequently. This is probably due to the increasing popularity of hard contact lenses. We may in time find that the wearing of hard con tact lenses, which is usually done for cosmetic reasons, may actually jeopardize beauty instead of improving it. Acknowledgments. The authors thank Willem Vreug denhil, MOptom, for recruiting the contact lens wearers, Bert Trenning, MD, for designing the data base, and Anne van Leeu wen, MD, for recruiting the control group.
References I. Jones LT, Quickert MH, Wobig JL. The cure of ptosis by · aponeurotic repair. Arch Ophthalmol 1975;93:629-34.
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear 2. Frueh BR. The mechanistic classification of ptosis. Oph thalmology 1980;87:1019-21. 3. Smith B, McCord CD, Baylis H. Surgical treatment of blepharoptosis. Am J Ophthalmol 1969;68:92-9. 4. Anderson RL, Dixon RS. Aponeurotic ptosis surgery. Arch Ophthalmol 1979;97: 1123-8. 5. Dortzbach RK, Sutula FC. Involutional blepharoptosis. A histopathological study. Arch Ophthalmol 1980;98:2045-9. 6. Anderson RL, Beard C. The levator aponeurosis: attach ments and their clinical significance. Arch Ophthalmol 1977;95: 1437-41. 7. Berlin AJ, Vestal KP. Levator aponeurosis surgery. A ret rospective review. Ophthalmology 1989;96: I 033-7.
8. Collin JRO. A Manual of Systematic Eyelid Surgery. Edin burgh: Churchill Livingstone, 1989;49-51. 9. Allansmith MR. Vernal conjunctivitis. In: Tasman W, Jae ger EA, eds. Duane's Clinical Ophthalmology, rev. ed. Phil adelphia: JB Lippincott, 1991. Vol. 4, chap. 9. 10. Allansmith MR, Ross RN. Giant papillary conjunctivitis. In: Tasman W, Jaeger EA, eds. Duane's Clinical Ophthal mology, rev. ed. Philadelphia: JB Lippincott, 1991. Vol. 4, chap. 9A. 11. Fonn D, Holden BA. Extended wear of hard gas permeable contact lenses can induce ptosis. CLAO J 1986;12:93-4. 12. Epstein G, Putterman AM. Acquired blepharoptosis sec ondary to contact-lens wear. Am J Ophthalmol 1981;91: 634-9.
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Purpose: The authors attempt to establish a relation between hard contact lens wear and upper eyelid ptosis. Methods: This study consists of two parts. In the first part, the authors compare the unilateral or bilateral ptosis that developed during hard contact lens wear in 17 patients with the involutional ptosis that developed in another group of 73 patients. In the second part, the authors compare both upper and lower eyelid position in 46 patients who had been wearing hard contact lenses for at least 10 years with the position of 50 matched controls who had never worn contact lenses. Results: The ptosis that had developed in the 17 patients who wore hard contact lenses was clinically similar to that caused by involutional levator disinsertion. The second part of the study shows that the prolonged wearers of hard contact lenses had upper eyelids that were lower by approximately 0.5 mm when compared with control subjects. This difference is statistically significant. According to standard criteria, there were at least 10 ptotic eyelids in the contact lens group versus 1 in the control group. Conclusion: The study findings suggest that prolonged hard contact lens wear may induce a lower position of the upper eyelid and eventually lead to ptosis through levator disinsertion. Ophthalmology 1992;99: 1759-1765
Disinsertion or thinning of the levator aponeurosis causes ptosis of the upper eyelid. 1-4 The commonest causes of levator disinsertion are trauma and involutional changes. The most frequent traumatic cause of disinsertion of the levator aponeurosis is intraocular surgery. 3 Traction on the eyelid during surgery, postoperative edema, and at teinpts made by the patient to open a patched eye after surgery all have been implicated as factors causing trau matic levator disinsertion. 2•3 In involutional ptosis, the process of aging causes thinning or disinsertion of the levator aponeurosis. Other factors that have been men tioned as possibly related to involutional ptosis through thinning or disinsertion of the levator aponeurosis are Originally received: March 13, 1992. Revision accepted: July 14, 1992. From the Eye Hospital Rotterdam, Rotterdam, The Netherlands. Reprint requests to Willem A. van den Bosch, MD, Eye Hospital Rot terdam, Schiedamsevest 180, 30 II BH Rotterdam, The Netherlands.
2 ocular inflammation and topically applied steroids. For brevity, we shall henceforth refer to any ptosis caused by thinning or disinsertion of the levator aponeurosis as apo neurogenic ptosis. The clinical picture of aponeurogenic ptosis of any cause is typical: the function of the levator muscle is good ( 12 mm or greater), and the ptotic eyelid shows a high skin crease. 2 .4,s The high skin crease develops because the posterior fibers of the levator aponeurosis on the tarsal plate disinsert or lengthen, while the anterior insertion of the levator aponeurosis into the orbicularis muscle and skin remains intact. 6 Occasionally, thinning of the eyelid can be observed. 2 The current treatment of choice of le vator disinsertion is the surgical reinsertion of the levator aponeurosis, if necessary combined with the reconstruc tion of the skin crease.I.3·4 •7•8 Thinning, disinsertion, or defects of the levator aponeurosis often can be recognized during surgical correction. 1 If it remains unclear whether a ptosis is aponeurogenic, other causes, such as inflammatory disorders of the con
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junctiva, muscular dystrophies, and neurologic disease, must be ruled out. 3 •6 •9 • 10 In addition, blepharospasm, pos sibly caused by photophobia secondary to conjunctivitis, must be excluded. 9·' 0 Ptosis caused by both vernal and giant papillary conjunctivitis also has been described. 9· 10 Importantly, hard contact lens wear as a possible cause of ptosis without tarsal conjunctival changes has, to our knowledge, only been reported twice. Its pathogenesis, however, remains a mystery. In one report, ptosis devel oped within a few weeks when habitual, daily-wear contact lens wearers exchanged their hard or soft lenses for ex tended-wear hard lenses. In these cases, the ptosis disap peared within a few weeks after switching back to the previous, daily-wear lens type. 11 This reversibility pre cludes that the ptosis in these cases was aponeurogenic. In another series, five patients with eight ptotic eyelids were described. 12 These patients had both the clinical and the intraoperative signs of ptosis through levator disin sertion. In the first part of the current report, we confirm and extend these reports by describing 17 patients who de veloped a ptosis while wearing hard contact lenses for at least 3 years. To further investigate the relation between prolonged wearing of hard contact lenses and ptosis, we examined a group of habitual wearers of such lenses and compared the position of their eyelids with that of a matched control group. None of the contact lens wearers complained of any ptosis. We found that the position of the upper eyelid was indeed lower by approximately 0.5 mm in the contact lens wearers group compared with the controls. Some of the data ofour asymptomatic hard con tact lens wearers even satisfied the set criteria of ptosis. Our findings strongly support the notion that hard contact lenses play a role in the development of ptosis through levator disinsertion.
Patients with Contact Lens Related Ptosis Patients and Methods Between January 1990 and November I99I, I7 long-term wearers of hard contact lenses sought treatment for bleph aroptosis that had developed in one or both upper eyelids. All patients were carefully examined to assess the cause of their ptosis. Levator function was 12 mm or more in all cases. If the ptosis was severe, the skin crease was high. We did not observe any signs of congenital ptosis, such as lid-lag on downgaze. No abnormalities of the tarsal plate or upper fornix, which could have caused the ptosis, were seen. No signs indicative of a muscular or neuro muscular disorder that might cause the ptosis, such as lid twitch or worsening of the ptosis after sustained upgaze, were found. None of these patients had photophobia or excessive blinking, which might possibly be associated with blepharospasm due to conjunctivitis. 9•10 On slit-lamp examination, all corneas were clear. In conclusion, we found no abnormalities other than ptosis that, on clinical examination, showed the picture of aponeurogenic ptosis.
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All but 2 patients stated that the ptosis had developed gradually during the last I or 2 years, and most patients could illustrate this with photographs. In the other 2 pa tients, the ptosis had existed for 6 and 16 years, respec tively, and had become gradually worse. The patients were between 18 and 56 years ofage (mean age, 38.5 years). There were 14 females and 3 males. Fif teen of the patients wore hard contact lenses bilaterally; one patient wore only one hard contact lens and had a ptosis on that side, whereas another patient wore a hard lens on one side, and a soft lens on the other. She had a ptosis on the side in which the hard lens was worn. In total, 32 hard contact lenses were worn in our group. The wearing time of the lenses varied from 3 to 27 years (mean wearing time, 15.2 years). Two patients used a suction cup to remove the hard contact lenses from their eyes. All other patients removed their lenses by blinking force fully while pulling their eyelids laterally. All patients were photographed with a camera mounted with a 135-mm macro lens. The patients were asked to look at the lens center when the pictures were taken. These pictures were later used to measure the upper eyelid height. The height ofthe upper eyelid was expressed in millimeters as the upper margin reflex distance, which was, by defi nition, the distance between the center of the pupil and the lower margin of the upper eyelid. The horizontal cor neal diameter served as a calibration reference for the measurements; it was assumed to have a magnitude of 11.8 mm, since this was the average value found in the second part of this study (see below). The photographs of 3 patients are shown in Figures 1 to 3. Figure 1A shows the typical clinical picture of a bilateral ptosis through levator disinsertion of a 47-year old patient who had worn hard contact lenses for 24 years. Figure IB shows the same patient 1 week after successful surgical anterior levator reinsertion. Figure 2 shows a 23 year-old patient who developed a right-sided ptosis after 6 years of bilateral hard contact lens wear. Figure 3 shows a 23-year-old patient who had been wearing a hard contact lens on the right side and a soft contact lens on the left side for 7 years; note that she had developed a ptosis on the side of the hard contact lens.
Results The upper margin reflex distances of all 34 eyelids in our I7 patients are depicted in Figure 4. For a clear assessment of these data, we have set a criterion for ptosis at an upper margin reflex distance of less than 2.8 mm. This value equals the mean upper mar gin reflex distance minus twice its standard deviation as found in control subjects in the second part of our study, to be described. For clarity, we have added a line in Figure 4, which represents the criterion of 2.8 mm. According to this criterion, there were 24 ptotic eyelids in our study. If we include 1 more patient who had an upper margin reflex distance of more than 3 mm, but who showed an asymmetry of 2 mm between the two upper eyelids, there were 25 cases.
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear
Figure 1. A, a typical, 47-year-old patient who had been wearing hard contact lenses for 24 years. Her bilateral ptosis with high skin crease is prominent. B, 1 week after anterior levator reinsertion.
To date, surgical correction has been performed in I 0 patients. This was done by reinserting the levator apo neurosis on the anterior surface of the tarsal plate under local anesthesia and reconstructing the skin crease. 8 Dur ing surgery, we observed disinsertion of the levator apo neurosis in both upper eyelids of one patient and a very thin levator aponeurosis in both upper eyelids offive other patients. The operative procedure was successful in all I0 patients. To distinguish this group from another group of pa tients with involutional ptosis, we compared the age dis tribution of the first group with that of a group of 73 patients with involutional ptosis who were seen in the eyelid clinic during the same period. In this group, no reasons other than levator disinsertion secondary to in volutional changes were present (i.e., no previous intra ocular or eyelid surgery, no contact lens wear, etc.). They were between 48 and 88 years ofage (mean age, 69 years). Figure 5 shows the age distribution of the two groups. There is only a slight overlap in age between the two groups, which strongly suggests that disinsertion of the levator aponeurosis associated with hard contact lens wear is a distinct category.
Figure 2. A 23-year-old patient who had developed a right-sided ptosis during 6 years of bilateral hard contact lens wear.
Eyelid Position After Prolonged Hard Contact Lens Wear Compared with a Matched Control Group Subjects and Methods In the first part of this study, we demonstrated that apo neurogenic blepharoptosis may be associated with pro longed use of hard contact lenses. It is as yet unclear whether a lowering of the upper eyelid occurs in all hard contact lens wearers or whether this will happen only in susceptible individuals. Therefore, we photographed and investigated 50 consecutive patients at our contact lens department who had been wearing hard contact lenses in both eyes for at least 10 years (average period, 16.3 years). These patients were matched for age and sex with 50 con trols. In the contact lens group, the mean age was 35.4 years with a standard deviation (SD) of 7.5 years. The mean age of the control group was 35.6 years with an SD of7.4 years. Everyone in either group had a bilateral visual acuity of 20/20 or better with optical correction (contact
Figure 3. A 23-year-old patient who had been wearing a hard contact lens on the right and a soft contact lens on the left side for 7 years. She had developed a ptosis on the side of the hard contact lens.
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lenses or spectacles), if required. In both groups, exclusion criteria were any corneal pathology, any ophthalmologic operation, family history of ptosis, any previous ocular inflammatory disease, use of eyedrops, and diseases that might influence eyelid position (allergies, hay fever, facial palsy, Graves disease, neurologic and muscle diseases). After obtaining informed consent and a detailed his tory, the eyelids were photographed. To photograph the subjects, we used a chin rest and instrument table previ ously used for a keratometer. On the instrument table, a camera with a 50-mm macro lens and a flash unit were fitted instead of the keratometer. The focal distance of the lens was fixed at 30 em. Eight photographic slides were taken of each contact lens wearer: two of each eye while wearing the contact lens and two ofeach eye shortly after removing the contact lens. In the control group, two photographic slides of each eye were taken. To obtain comparable measurements, great care was taken to align the optical axis of the camera with the corneal center, and each subject was requested to look at the center of the camera lens. After photographing the eyes, we everted the upper eyelids. Subjects with abnormalities of the tarsal plate (follicles, papillary conjunctivitis, scars) were excluded from our study. The slides were projected onto the screen of an Agfa Copex LP3 projector (Agfa Gevaert, Leverkusen, Ger many), which produced a magnification of six times life size. The corneal center was determined by centering a set of concentric circles on the pupil. On each slide, the horizontal corneal diameter and the upper margin reflex distance were measured. In addition, the distance between pupil center and lower eyelid margin was measured. These measurements all were performed by the same technician, who was not aware of the working hypothesis of the study. The measurements on the individual slides were repro 7 6
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ducible with an accuracy better than 0.15 mm. Two slides were available for each measurement; their averaged re sults served as final data for each eyelid. From the contact lens group, the results from four pa tients could not be used for several reasons. Thus, mea surements of only 46 patients (92 eyes) were used for this study. In the control group, results from all 50 subjects were used.
Results The upper eyelid margin was, on average, 0.5-mm lower in hard contact lens wearers than in subjects in the control group (P < 0.0015, Wilcoxon rank sum test). Figure 6A shows the distribution ofthe upper margin reflex distance both in the contact lens wearers and in the control subjects. It is evident from Figure 6A that the distribution of the upper margin reflex distance in the contact lens wear ers is shifted toward a lower (i.e., more ptotic) position compared with the control subjects. In the control group, the mean upper margin reflex distance was 4.2 mm (SD = 0.7 mm), while in the contact lens wearers group it averaged 3.7 mm (SD = 1.0 mm). Shortly after the hard contact lenses were removed, the position of the upper eyelids did not change significantly (Figs 6A and 6B). Be cause the upper margin reflex distance distribution in the control group assumes a pseudo-Gaussian curve, we de termined a standard criterion for ptosis by subtracting twice the standard deviation from the mean upper margin reflex distance. This standard criterion equaled 2.8 mm (4.2- [2 X 0.7]). For clarity, we have drawn a line at this criterion of 2.8 mm in Figures 6A and 6B. Adopting this criterion, we found 10 ptotic eyelids in the hard contact lens group while wearing the lens, and 1 more shortly after the lenses were removed. In contrast, there was only 1 ptotic eyelid in the control group. Note that none of our 96 subjects complained of any ptosis. Figures 7A and 7B show the lower margin reflex dis tances (i.e., the distance between the pupil center and the
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear
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Figure 6. Frequency distribution of upper eyelid position (expressed as U-MRD) in the hard contact lens wearing group (black bars) and in the control group (white bars). A, contact lens group wearing hard contact lenses; B, shortly after contact lens removal. The horizontal line indicates the criterion for ptosis of 2.8 mm.
lower eyelid margin) ofthe hard contact lens wearers both with their lenses in and shortly after lens removal, re spectively. For comparison, the data of the control group are also presented in the same figures. No significant dif ference in lower eyelid position was found between contact lens wearers and the control group. Also, no significant difference in lower eyelid position was found in the contact lens group between measurements during hard contact lens wear and measurements after lens removal. The av erage lower margin reflex distance was 5.8 mm before lens removal (SD = 0.8 mm), and also 5.8 mm (SD = 0.7 mm) after lens removal.
Discussion To date, detailed reports on ptosis associated with the long-term wearing of hard contact lenses have been fairly scarce. We have tried to fill the gap somewhat by reporting on 17 patients with such a ptosis. This hard contact lens related ptosis resembled clinically the picture of a ptosis due to disinsertion or thinning of the levator aponeurosis.
Moreover, such thinning or disinsertion was actually ob served in several of our operated patients. We ruled out the possibility that our results were confounded by other, well-known, causes of levator thinning or disinsertion, such as surgical trauma or involutional, degenerative changes. Our study of eyelid position in normal, habitual, long term hard-contact lens wearers shows clearly that the up per eyelid may sag approximately 0.5 mm compared with matched controls. This has, to our knowledge, not been reported previously. Importantly, even a considerable number of our asymptomatic, long-term wearers of hard contact lenses had actually developed an outright ptosis. Perhaps the sagging of the upper eyelid develops so slowly in habitual wearers of hard contact lenses that it passes unnoticed for a long period of time. These results bring up the question how the wearing of hard contact lenses may bring about such changes to the levator aponeurosis. It is generally accepted that ex cessive traction on the upper eyelid, such as occurs with ocular surgery or with eyelid edema, may result in a dis insertion of the levator aponeurosis. 2 Most of our contact
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Figure 7. As Figure 6, for lower eyelid position.
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lens wearers took out their lenses by pulling the eyelid laterally. This traction is essentially different from the or thogonally directed traction associated with ocular surgery and edema. Therefore, one would expect this to cause a disinsertion, if any, of the lateral canthal ligament or me dial canthal tendon, but not of the levator aponeurosis proper. However, this practice of lens removal may still play a significant role in thinning or disinserting the levator aponeurosis: while the eyelid is pulled laterally the patient squeezes the lens out by blinking. Possibly, both the or bicularis and the levator muscle then contract simulta neously, because the eye has to be wide open, while a powerful blink is made. This antagonistic action of the orbicularis and levator muscle might exert increased trac tion on the levator aponeurosis, finally leading to its dis insertion. The same procedure of! ens removal also might damage the levator aponeurosis through another mechanism. If the attempt to remove a lens fails, the lens presumably will rub forcefully over the palpebral conjunctiva, thereby stretching it and the underlying structures, such as the levator aponeurosis. We therefore speculate that failed attempts to remove a hard contact lens by sideward pulling of the eyelids and blinking may yield disinsertion or thin ning of the levator aponeurosis. These mechanisms may have played a role in the series described by Epstein and Putterman. 12 Of the five patients who developed a ptosis during hard contact lens wear, two patients developed the ptosis directly after they were fitted with hard lenses. The ptosis in these cases was not reversible. Obviously, the use of a suction cup to remove the lenses would not have this effect. Interestingly, there were two patients in our study who used a suction cup for lens removal who had nonetheless developed a ptosis. Therefore, at least one other mecha nism should be held responsible for the sagging of the upper eyelid in some hard contact lens wearers. One might argue that every blink made during the reg ular wearing of hard contact lenses rubs the lens against the eyelid structures. This repeated rubbing may finally cause levator disinsertion much in the same way as de scribed above. In this mechanism, the way in which the contact lenses are fitted, as well as the position of the contact lens on the eyeball, may play a role. We did not investigate these aspects in our patients, although they might, in future, be of great potential interest. Also, irritation ofthe eyelid by the lens may cause eyelid edema and ptosis due to the force of gravity. This ptosis would be reversible in a beginning stage, since discontin ued wearing of the lens would take away the irritation, allowing the eyelid to slim to its original proportions. It may be that this mechanism played a role in the cases described by Fonn and Holden, 11 who fitted 11 long-term wearers of hard or soft contact lenses with an extended wear hard contact lenses in one eye. Approximately half of their group developed a ptosis within 4 weeks, which again disappeared within 2 to 4 weeks after cessation of wearing the extended-wear lens. 11 Irritation might not only produce swelling and subse quent ptosis, it also might induce reflex blepharospasm.
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This could, along similar lines, account for the ptosis ob served by Fonn and Holden .'' In addition, it could be responsible for the ptosis in our patients, as well as for the lower position of the upper eyelid observed in our long-term wearers of hard contact lenses. Prolonged spasm of the orbicularis could strain the levator muscle or could cause, in turn, a higher tonus of the levator muscle. Blepharospasm would not only cause a lower position of the upper eyelid, but also a higher position of the lower eyelid. Interestingly, we did not find a difference in lower eyelid position between long-term lens wearers and con trols. Also, there was no change in upper eyelid position directly after lens removal. Therefore, blepharospasm ap pears to be a less likely cause of sagged upper eyelids in wearers of hard contact lenses. In summary, at least five different mechanisms can be tentatively put forward through which disinsertion and thinning of the levator aponeurosis in hard contact lens related ptosis may possibly come about. These are: (1) simultaneous, although antagonistic, action of the orbi cularis and levator muscle while squeezing the eyelids to remove the lens; (2) forceful rubbing of the lens and sub sequent stretching of upper eyelid structures during failed attempts of lens removal; (3) repeated and similar, al though less forceful, rubbing of the lens during blinking; (4) irritation, leading to edema; and (5) irritation leading to blepharospasm. It is, as yet, not clear to what extent these presumed mechanisms add, if anything, to the ptosis. Our results bring up another interesting question. Does the hard contact lens-related ptosis develop only in sus ceptible individuals, or does every wearer of such lenses eventually run an equal risk? We have reported, for the first time, that habitual wearers of hard contact lenses have upper eyelids that sag, on average, 0.5 mm compared with matched controls. We do not know, however, to what extent this sagging is reversible or by what mechanism it is caused. If it were reversible, this would surely be of great interest to those with marked sagging. We have in sufficient evidence to attribute this sagging to a thinning or disinsertion of the levator aponeurosis. Such a possi bility, however, by the same token, cannot be excluded. Prolonged wearing of hard contact lenses will nonetheless lead, in some individuals, to a ptosis due to damage to the levator aponeurosis. Importantly, we believe that we come across such ptosis ever more frequently. This is probably due to the increasing popularity of hard contact lenses. We may in time find that the wearing of hard con tact lenses, which is usually done for cosmetic reasons, may actually jeopardize beauty instead of improving it. Acknowledgments. The authors thank Willem Vreug denhil, MOptom, for recruiting the contact lens wearers, Bert Trenning, MD, for designing the data base, and Anne van Leeu wen, MD, for recruiting the control group.
References I. Jones LT, Quickert MH, Wobig JL. The cure of ptosis by · aponeurotic repair. Arch Ophthalmol 1975;93:629-34.
van den Bosch and Lemij · Blepharoptosis Induced by Hard Contact Lens Wear 2. Frueh BR. The mechanistic classification of ptosis. Oph thalmology 1980;87:1019-21. 3. Smith B, McCord CD, Baylis H. Surgical treatment of blepharoptosis. Am J Ophthalmol 1969;68:92-9. 4. Anderson RL, Dixon RS. Aponeurotic ptosis surgery. Arch Ophthalmol 1979;97: 1123-8. 5. Dortzbach RK, Sutula FC. Involutional blepharoptosis. A histopathological study. Arch Ophthalmol 1980;98:2045-9. 6. Anderson RL, Beard C. The levator aponeurosis: attach ments and their clinical significance. Arch Ophthalmol 1977;95: 1437-41. 7. Berlin AJ, Vestal KP. Levator aponeurosis surgery. A ret rospective review. Ophthalmology 1989;96: I 033-7.
8. Collin JRO. A Manual of Systematic Eyelid Surgery. Edin burgh: Churchill Livingstone, 1989;49-51. 9. Allansmith MR. Vernal conjunctivitis. In: Tasman W, Jae ger EA, eds. Duane's Clinical Ophthalmology, rev. ed. Phil adelphia: JB Lippincott, 1991. Vol. 4, chap. 9. 10. Allansmith MR, Ross RN. Giant papillary conjunctivitis. In: Tasman W, Jaeger EA, eds. Duane's Clinical Ophthal mology, rev. ed. Philadelphia: JB Lippincott, 1991. Vol. 4, chap. 9A. 11. Fonn D, Holden BA. Extended wear of hard gas permeable contact lenses can induce ptosis. CLAO J 1986;12:93-4. 12. Epstein G, Putterman AM. Acquired blepharoptosis sec ondary to contact-lens wear. Am J Ophthalmol 1981;91: 634-9.
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