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4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs

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One in 10 ocular surgeries may result in ptosis. Here's how to
prevent it and how to treat it when you can't.
Alison v. Crum, ND
C. Robert Bernardino, ND, FACS
New Haven, Conn.
Ocular surgery, whether cataract, cornea, glaucoma or retina has evolved to become highly efficient and
predictable. However, complications can still occur, including corneal edema and decompensation, lens
subluxation, vitreous loss, macular edema and retinal detachment. Eyelid malposition can occur after
any ocular surgery including ectropion,1 entropion2 and ptosis. The incidence of ptosis after cataract
surgery has been reported to be as high as 13 percent3; the rate of entropion and ectropion after
cataract surgery is not known.
The cause of postoperative ptosis is manifold including postoperative edema, anesthesia and surgical technique. This article will
discuss the evaluation, etiology, treatment and prevention of ptosis after ocular surgery.

Ptosis can be divided into its etiologies, including myogenic, aponeurotic, neurogenic, mechanical or traumatic.+
Nyogenic ptosis is typically caused by congenital dysgenesis of the levator muscle or an acquired muscular dystrophy. !n post-
surgical myogenic ptosis, direct damage to the levator muscle may be due to the process of injecting anesthetic into the muscle or
myotoxic effects of the anesthesia.
Aponeurotic ptosis is a disinsertion or dehiscence of the levator aponeurosis from its normal position on the anterior surface of
tarsus. The use of a bridle suture or rigid lid speculum has been implicated in cataract surgery as a cause of aponeurotic damage.
Neurogenic ptosis is a disruption of the innervation of the muscle, and in the case of post-surgical ptosis, the prolonged effects of
anesthetic on the neuromuscular junction cause this transient phenomenon. This may also be caused by susceptibility of anteriorly
located terminal twigs of the oculomotor nerve to local anesthesia infiltrated in the eyelid in a van Lint block.5
Nechanical ptosis occurs when a mass causes downward pull on the upper eyelid. !n postoperative ptosis this may be due to edema
or hematoma formation in the eyelid. Finally, traumatic ptosis is due to blunt or sharp trauma to the levator aponeurosis. All of the
4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs
causes discussed in the categories above can be included under the heading of trauma.
Post-surgical ptosis is an acquired ptosis in which duration of the ptosis can help determine the etiology. Ptosis that resolves after
surgery is considered transient or acute ptosis; ptosis that persists after surgery is categorized as chronic or persistent.

Transient ptosis, or ptosis that improves over the postoperative
period, can be caused by eyelid edema, hematoma formation (both
intraorbital and eyelid), foreign body reaction, ocular inflammation
and anesthesia effects.
Postop edema is probably the most common cause of transient ptosis.
!t can be secondary to direct infiltration of anesthetic during an eyelid
block,6 or due to eyelid compression by the lid speculum against the superior orbital rim. Nost cases of eyelid edema will resolve
within +8 to 72 hours.7 Eyelid edema rarely persists past 10 days after surgery; the presence of ocular inflammation is typically the
cause of prolonged eyelid edema.8 Some authors speculate that the presence of lid edema may cause persistent ptosis by stretching
or dehiscing the levator aponeurosis9; other studies find no association between edema and ptosis after three to six months.
Hematoma formation, usually secondary to local injection of the eyelids during a van Lint block, is a form of mechanical ptosis.
However, even intraorbital hematoma secondary to peribulbar or retrobulbar anesthesia can cause limited function of the levator
muscle and secondary ptosis. Ocular massage or compression after injection can limit hematoma formation.10 Resorption of a
hematoma can cause fibrosis and adhesions between the orbital septum and levator aponeurosis and create persistent ptosis.
Foreign-body reaction is overlooked as a cause of ptosis. !n extracapsular cataract surgery, nylon sutures can erode through
overlying conjunctiva and cause inflammation and edema in the eyelid.11 Ocular inflammation and surface irritation after surgery
also create a transient, reactive ptosis. With correction of the inflammation, the edema and ptosis resolve.
Short, transient ptosis can occur as a direct response to the
neuromuscular blockade of the levator muscle. This can be secondary
to a retrobulbar or peribulbar block with anesthetic bathing the levator
complex. Furthermore, lid infiltration can affect distal fibers of the
oculomotor nerve. Choice of anesthetic can determine the duration of
ptosis, lidocaine having a shorter duration than bupivicaine.
The use of hyaluronidase can also alter the effects of local anesthetic;
it acts to increase the spread of anesthetic between tissue planes by
action of hyaluronic acid.12 No study has directly evaluated the effects
of hyaluronidase on postoperative ptosis, but increased availability of
anesthetic may increase the incidence of ptosis. Adjusting pH of the
anesthetic can also increase its availability; buffering an anesthetic
with bicarbonate can increase the pH of local anesthetic. Compared to hyaluronidase, anesthetic buffered with bicarbonate had a
higher rate of ptosis in one study. This may be due to increased availability of anesthetic with buffering or increased toxicity due to
the different pH.
Finally, ocular massage or compression can increase availability of anesthetic. Although it has been demonstrated to decrease lid
edema and hematoma formation, increased availability of anesthesia in the peribulbar or retrobulbar space can increase the rate of
4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs
!f ptosis persists past the neuromuscular effects of the anesthetic, one must suspect the myotoxic effects of anesthesia. One study
demonstrated that lidocaine causes degeneration of human muscle 18 hours after injection.13 Epinephrine heightens the myotoxic
effects of local anesthetic.1+ Recovery of muscle function and resolution of ptosis occur both due to regeneration of damaged muscle
fibers, and hypertrophy of remaining muscle fibers15; this process should take between eight and 12 weeks.16

Causes of persistent or chronic ptosis usually involve damage to the levator aponeurosis or scarring to the levator complex. Direct
damage to the muscle via toxic effects of anesthesia or trauma from direct injection of the muscle usually resolves with regeneration
of the muscle. Dehiscence or detachment of the levator aponeurosis from the tarsal plate does not remedy itself; therefore, this form
of ptosis does not improve over the postoperative period.
There are many factors implicated in the dehiscence of the levator
aponeurosis: prolonged lid edema, use of bridal sutures, and use of
lid speculum. George L. Paris, ND, and Narvin H. Quickert, ND,
were the first to hypothesize the cause of aponeurotic dehiscence
after ocular surgery.9 They felt that prolonged lid edema caused
disinsertion of the levator aponeurosis in older patients who have a
vulnerable aponeurosis. This pathogenesis is similar to that in
blepharochalasis and post-blepharoplasty patients with prolonged
eyelid edema. However, other studies have found no correlation between prolonged eyelid edema and ptosis.6,8
The use of a bridle suture during cataract surgery has also been implicated in post-surgical ptosis. Ptosis occurs both by grasping the
superior rectus during passage of the bridle suture and traction of the superior rectus by the bridle suture. Nichael Loeffler, ND, and
colleagues demonstrated that open visualization of the superior rectus, versus blind passage of the bridle suture by grasping the
superior rectus with forceps, decreases the amount of postoperative ptosis.17 The effect of the bridle suture is enhanced with the use
of a lid speculum. Traction on the superior rectusflevator complex while the upper lid is rigidly fixated with a speculum can cause
marked dehiscence of the aponeurosis.3 Jignesh Patel and colleagues, however, found no significant difference of ptosis
development in patients who had a bridle suture placed versus those who did not.18
Finally, the lid speculum has been indicated as a cause of persistent ptosis. The effects of the lid speculum are not dependent on the
use of a bridle suture. John Linberg, ND, and associates demonstrated ptosis after refractive surgery where a bridle suture is not
used.19 The authors speculate that use of a rigid speculum versus a flexible wire speculum may cause dehiscence of the aponeurosis
when the lid is forcefully squeezed or blinked; a wire speculum will yield to such forces.

After a thorough examination in which the etiology is determined, one must decide whether to intervene. !n most cases, post-surgical
ptosis resolves with time, and therefore observation is the most prudent form of intervention. As in other forms of traumatic ptosis,
this form of ptosis typically improves within six months. Fereydoun Parsa, ND, and associates reported a case of spontaneous
resolution of ptosis after 11 months and suggest observing post-surgical ptosis for one year.20
Ptosis that does not resolve is typically secondary to aponeurotic dehiscence; this is readily repaired surgically. However, prior to
considering surgical intervention, one must determine whether the patient is affected by the ptosis. !n one study, only 18 percent of
patients with postoperative ptosis noticed a change in their eyelid postion.8 Finally, plans for contralateral ocular surgery have to be
determined. !f a patient is planning ocular surgery in the other eye, surgical intervention for ptosis should be delayed, since the
second eyelid is at similar risk for postoperative ptosis.
4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs
Ptosis after ocular surgery is amenable to repair via an external approach through the lid crease and repair of the aponeurotic
dehiscence or a transconjunctival approach with Nellerectomy for minimal ptosis. The former approach is more logical since it
directly addresses the dehiscence of the levator aponeurosis. Furthermore, patients with a dehisced levator will have an increased lid
crease height and a superior sulcus defect secondary to retraction of the preaponeurotic fat pad. External levator resection through
the anatomic lid crease addresses all these problems; an internal approach does not. However, for minimal ptosis of 1 to 2 mm, a
Nellerectomy may be appropriate.

Prevention of post-surgical ptosis is an essential part of modern ocular surgery. Even if a patient obtains excellent visual acuity from
cataract surgery, a patient's function may be limited by post-surgical ptosis. Therefore, a surgeon should take an active role in
preventing this problem.
The choice of anesthesia can determine whether the levator is exposed to risk of developing ptosis. Topical anesthesia eliminates all
problems with local anesthesia including hematoma and edema of the eyelid and myotoxic effects on the levator. !f lid akinesis is
needed, a Nadbath retroauricular block is better than a van Lint eyelid block. !f ocular akinesis is required, a theoretical advantage
may exist with peribulbar anesthesia versus retrobulbar anesthesia with less direct damage to the muscles. However, two did not find
a significant difference between these two forms of anesthesia.8,21 The use of ocular massage and compression may decrease the
amount of eyelid edema and hematoma formation, but may increase the amount of anesthesia available for myotoxicity. The use of
hyaluronidase is also controversial; it may limit the amount of anesthesia volume needed but may increase the distribution of
anesthesia around the levator complex.
Surgical technique can also determine exposure to risk factors for post-operative ptosis. An efficient surgeon can limit surgical time
and thus eyelid complications secondary to ocular inflammation or compressive effects of prolonged use of a lid speculum. Also,
disuse of bridle sutures or a rigid speculum will limit these factors in ptosis. !f a bridal suture is necessary for fixation of the globe,
direct visualization of the superior rectus with dissection through conjunctiva and Tenon's capsule during placement of the bridle
suture will limit damage to the levator complex. An episcleral or corneal traction suture may also be considered. Use of a flexible wire
speculum and limiting the spreading tension on the eyelids may also limit postoperative lid malposition. !f a rigid speculum is
required, lid akinesia with anesthesia might limit aponeurotic damage.
Surgical technique may also decrease the incidence of ptosis; one study found a higher incidence of ptosis in extracapsular cataract
extraction versus phacoemulsification at eight weeks.6 However, there was no difference at six months after surgery. This difference
may be due to a larger conjunctival flap and scleral incision, as well as more sutures needed in wound closure, increasing the
likelihood of postop inflammation. With the advent of temporal, clear corneal surgery, these factors are reduced. One can also
speculate that the superior approach to surgery may have a greater risk of ptosis compared to a temporal approach, since vertical
traction of the globe during a superior approach may cause dehiscence of the aponeurosis, whereas a temporal approach has no
vertical vectors applied to the globe.
Lid malposition after ocular surgery should be recognized as a preventable complication. Understanding the causes of eyelid
malposition after surgery can help a surgeon prevent its occurrence with careful surgical planning. When present after surgery, a
thorough examination can help determine when, and if, surgical intervention is indicated. Finally, patients should be educated about
its possibility as a complication in routine ocular surgery.
Drs. Crum and Bernardino are at the Yale School of Nedicine, Department of Ophthalmology, Section of Ophthalmic Plastics and
Orbital Surgery. Contact Dr. Bernardino at Yale Eye Center, +0 Temple Street, 3D, New Haven, Conn. 06510. Phone: (203) 785-
2020; fax: (203) 785-5909; e-mail:

1. Hosal BM, Grsel TE. Eyelid malpositions after cataract surgery. Euro J Ophthalmol 199S;S:12-15.
4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs
2. Hurwitz JJ, Smith D, Corin SM. Association of entropion with cataract surgery. Ophth Plast Reconstr Surg
3. Alpar JJ. Acquired ptosis following cataract and glaucoma surgery. Glaucoma 19S2;466-6S.
4. Beard C. Ptosis, 3rd ed. St. Louis: Mosby, 19S1.
5. Hwang K, Lee DK, Chung IH, Lee SI. Patterns of oculomotor nerve distribution to the levator palpebrae
superioris muscle, and correlation to temporary ptosis after blepharoplasty. Ann Plast Surg 2001;47:3S1-3S4.
6. Kaplan LJ, Jaffe NS, Clayman HM. Ptosis and cataract surgery. A multivariant computer analysis of a prospective
study. Ophthalmol 19S5;92:237-242.
7. Wolfort FG, Poblete JVP. Ptosis after blepharoplasty. Ann Plast Surg 1995;34:264-267.
S. Feibel RM, Custer PL, Gordon MO. Postcataract ptosis. A randomized, double-masked comparison of peribulbar
and retrobulbar anesthesia. Ophthalmol 1993;100:660-665.
9. Paris GL, Quickert MH. Disinsertion of the aponeurosis of the levator palpebrae superioris muscle after cataract
extraction. Am J Ophthalmol 1976;S1:337-340.
10. Ropo A, Ruusuvaara R, Paloheimo M, Maunuksela EL, Mikki P. Periocular anaesthesia: Technique, effectiveness
and complications with special reference to postoperative ptosis. Acta Ophthalmologica 1990;6S:72S-732.
11. Shahinian L, Brown SI. Postoperative complications with protruding monofilament nylon sutures. Am J
Ophthalmol 1977;S3:546-54S.
12. Mather C, Smith JH, Bloom PA. The efficacy of 0.75% bupivicaine with ph adjustment and hyaluronidase for
peribulbar blockade: the incidence of prolonged ptosis. Euro J Ophthalmol 1994;4:13-1S.
13. Yagiela JA, Benoit PW, Buoncristiani RD, et al. Comparison of myotoxic effects of lidocaine with epinephrine in
rats and humans. Anesth Analg 19S1;60:471-4S0.
14. Yagiela JA, Benoit PW, Fort NF. Mechanism of epinephrine enhancement of lidocaine induced skeletal muscle
necrosis. J Dent Res 19S2;61:6S6-690.
15. Rainin EA, Carlson BM. Postoperative diplopia and ptosis. A clinical hypothesis based on the myotoxicity of local
anesthetics. Arch Ophthalmol 19S5;103:1137-1339.
16. Rao VA, Kawatra VK. Ocular myotoxic effects of local anesthetics. Can J Ophthalmol 19SS;23:171-173.
17. Loeffler M, Solomon L, Renaud M. Postcataract extraction ptosis: Effect of the bridle suture. J Cataract Refract
Surg 1990;16:501-540.
1S. Patel JI, Blount M, Jones C. Surgical blepharoptosisthe bridle suture factor? Eye 2002;16:535-537.
19. Linberg JV, McDonald MB, Safir A. Googe JM. Ptosis following radial keratotomy. Ophthalmol 19S6;93:1509-
20. Parsa FD, Roach JM. A case report on spontaneous return of levator function following postcataract
blepharoplasty repair. Ann Plast Surg 1996;37:63S-649.
21. Kawa P, Siwek M, Mankowska A, Zagorski Z. Postoperative ptosis after cataract extraction: own material. Klin
Oczna 2000; 102: 25-2S.
4]2]12 RevIew oI OphthaImoIogy > PreventIng & ManagIng Post-SurgIcaI PtosIs
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